October 2013

(Last updated December 2017)

Collated by Henry Bauer

Additions and corrections are welcomed,
indeed solicited, at our comments page.

That HIV causes AIDS has been the officially sanctioned view for about 3 decades, believed almost universally but questioned openly by thousands of people, some of whom are expert in relevant sciences 1,2,3. These dissidents point out that a comprehensive reading of the mainstream literature together with analysis of mainstream data demonstrates conclusively that HIV is neither a necessary nor a sufficient cause of AIDS. An up-to-date and comprehensive yet concise summary of the facts and the history of the HIV/AIDS blunder is provided by Donald Miller 914.

An annotated bibliography of dissident books and other writings was published in 1993 4; dissident books not listed there or published since that time include Bauer 5, Bialy 6, Crewdson 7, Culshaw 8, De Harven 9, Duesberg 10, Farber 11, Fiala 12, Hodgkinson 13, Konotey 14, Kremer 15, Lauritsen 16, Lauritsen & Young 17, Leitner 18, Maggiore 19, Root-Bernstein 20, Shenton 21.

The Immunity Resource Foundation (IRF) offers important archival material including many documentary films and videos; many issues of Continuum magazine; many links to other AIDS-Rethinking or HIV-Skeptical websites; and a blog and newspage. The 2013 award-winning film, “Positively False — Birth of a Heresy” can be rented or bought at the IRF website. Another award-winning documentary is "House of Numbers."

At first sight, that HIV does not cause AIDS must seem unbelievable in light of the officially promulgated view that has so thoroughly pervaded the media and the public sphere. How could medical science be so wrong for so long about something so important? Moreover, haven’t the miracle antiretroviral drugs (ARVs) saved countless lives and changed AIDS from an invariably fatal death sentence into a chronic, manageable, condition? Aren’t Africans dying in hordes from AIDS only because they can’t get enough of those drugs?

Those questions can all be answered, but not in any brief way. The comprehensive case against HIV has to be made along several mutually reinforcing lines:

  1. Questions to which the officially sanctioned view has no answer.
  2. HIV does not cause AIDS.
  3. The plain evidence about AIDS.
  4. The plain evidence about HIV.
  5. Failings of HIV/AIDS theory.
  6. What antiretroviral drugs do.
  7. Damage done by HIV/AIDS theory and practice.
  8. Hindrances to making the case against HIV.
  9. How could such a massive blunder come about and persist?
  10. FAQs: Questions — sometimes rhetorical only — posed by adherents to HIV/AIDS theory.

Just how inconceivable most people find it, that HIV/AIDS theory could be so wrong, that official medicine and science could be so wrong in this day and age, may be illustrated by my own experience 514. I had read enough — many of the books listed above — to become open to the possibility, but it took my own digging into “HIV” epidemiology to convince me p.7 & chapter 1 in 5, and that was about 10 years after I first became aware that there exist dissidents from orthodox HIV/AIDS belief. And it has taken me further years to understand that “HIV” may not even exist, and that “HIV” tests are perhaps the central issue in the whole business. My long-standing interest in Loch Ness Monsters and the like testifies that I am significantly more open to unorthodox views than are most people, so my own difficulty in recognizing the errors of HIV/AIDS theory might serve as a warning, that the task of bringing others to that understanding is an extraordinarily difficult one.

(The Footnotes include many URLs. Those beginning with “” refer to the blog by Henry Bauer at; the blog posts include further citations to the mainstream literature. URLs that were not active when this document was drafted show the date when that URL was last accessed directly; such broken links can often still be found indirectly via the Wayback Machine 22, or sometimes a copy of the source can be found via a Google search on the article’s title.)


0.1 Why is there no gold-standard test for HIV infection? 127

0.1.1 [Because authentic pure HIV virions have never been isolated from supposedly infected individuals nor have they ever been successfully synthesized (cloned) — see section 3.1.3]

0.2 How does HIV supposedly destroy the immune system? (see sections 1.3.3, 4.4.4)

0.3 Why do people of African ancestry test "HIV-positive" more than all others, whether in Africa or America or Europe? chapters 5-7 & p. 106 in 5

0.4 Why were AIDS and HIV first identified in America and Europe when HIV is supposed to have first infected human beings in Africa? (see section 4.6)


1.1 It was never established in the first place, nor later proved, that HIV causes AIDS.

1.1.1Kary Mullis has described his unsuccessful quest — including asking the discoverer of HIV — for citations to the scientific articles that prove HIV to be the cause of AIDS 23.

1.1.2The “fact sheets” issued by the National Institutes of Health are not scientific articles, and their claims of proof have been refuted in full detail 24,25. Those refutations have been ignored or misrepresented but never effectively challenged.

1.1.3The issue is complicated by progressive re-definitions of AIDS, see section 2.

1.1.4Luc Montagnier, credited with the discovery of HIV, reported that AIDS seemed to be caused by a mycoplasma and not by HIV 26,27,28,29,30,31.

1.1.5By 1993 so many cases of “HIV-negative” “AIDS” had been reported 32,33,34,35 that the condition was pronounced a new disease, “idiopathic CD4 T-cell lymphopenia” (ICL) 36,37,38,39,40,41,42,43 (also “HIV-negative adult-onset immunodeficiency” 44): immune deficiency of unknown cause with low CD4 counts; but this is precisely the same as the original definition of AIDS.

1.1.6“HIV-positive” individuals do not necessarily ever progress to AIDS in absence of any treatment 45. Co-factors in addition to HIV required to bring on AIDS have been postulated on a number of occasions: mycoplasma 26,27,28,29,30,31; HTLVs page 248 in 257; cell surface protein CD26 871,872; the protein fusin 873.

1.1.7Specific Italian data illustrate that HIV does not cause AIDS 46,47,48.

1.2HIV and AIDS are not even correlated.

1.2.1The seminal papers claimed to have found the putative retrovirus in only “18 of 21 patients with pre-AIDS … [and] 26 of 72 adult and juvenile patients with AIDS” 49. This did not even establish that HIV is correlated with AIDS 50, let alone causes it. The principal author, Robert Gallo, may have committed scientific misconduct as well 7,51,648. of those who refer to the discovery of HIV credit Montagnier, not Gallo 52.

1.2.2Kaposi’s sarcoma (KS) was one of the three originally iconic AIDS diseases, yet HIV-negative cases of KS had been noted at the very beginning 53 and turned out to be quite common 54. is now ascribed not to HIV but to something else 64, perhaps KSHV (Kaposi’s sarcoma herpes virus) or HHV-8 (human herpes virus 8) 55,56,57,58. AIDS-1 (section 2.1) KS was probably caused by the widespread use of nitrite “poppers” by many gay men 59,60,61,62,63,64. Although described as a cancer (sarcoma), it may actually be non-malignant damage to blood vessels.

1.2.3HIV and AIDS are not correlated with respect to geography chapter 9 in 5,80.

1.2.4HIV and AIDS are not correlated with respect to race chapter 9 in 5.

1.2.5HIV and AIDS are not correlated with respect to the sexes chapter 9 in 5.

1.3HIV does not even cause illness, let alone death 66,45.

1.3.1The mortality of “HIV-positive” individuals and of “People with AIDS” (PWAs) is independent of age whereas mortality increases very significantly with age in every (other) illness 67,68,69,70,71.

1.3.2About 50% of people testing “HIV-positive” never experience illness associated with “HIV” 72,73,74.

1.3.3It remains mysterious, in what way or by what mechanism HIV could cause illness of any kind; a number of mechanisms have been bruited, none has been demonstrated or accepted as satisfactory 75.“HIV” is found in only a tiny proportion (<1%) of the T-cells that it supposedly kills, so the decrease in CD4 counts supposedly characteristic of AIDS or “HIV disease” is ascribed to an unspecified “bystander mechanism” 833,866,867,868. long ago argued that no retrovirus could act as claimed for HIV 76.


Which AIDS?

AIDS has been defined in at least three distinctly different ways at different times and in different places. To avoid confusion, it is necessary to distinguish among them as AIDS-1, AIDS-2, and AIDS-Africa.

2.1The first definition of AIDS, therefore AIDS-1: A supposedly unprecedented syndrome characterized by immune deficiency (specifically, low CD4 counts) of unknown cause presumed responsible for the presence of manifest opportunistic infections, chiefly Kaposi’s sarcoma, Pneumocystis carinii pneumonia (PCP), or candidiasis (fungal: thrush, yeast infection) 77,78.

2.1.1Designating AIDS-1 as a new medical phenomenon was an error because of the “AIDS-1” diseases was previously unknown. They occur in HIV-negative individuals for a wide range of reasons 79. great many conditions and infections induce immune deficiency, even specifically the low counts of CD4 cells purported to be characteristic of AIDS — non-specific conditions like oxidative stress 80,15 (see also sections 3.2.2,,,, or such specific diseases as tuberculosis 82,83. initial diagnosis 103 was by a young physician early in his career who also had access to the relatively new technique of counting CD4 cells 84. However, we now know that CD4 counts are not a valid measure of good or bad health 897. In particular, “recreational” drugs 85,86,87,88,89,90 including nitrites (“poppers”) 91,92 cause the same conditions as are said to be characteristic of AIDS, including loss of CD4 cells 93, and drug addicts display the same manifest symptoms as were ascribed to AIDS-1 13. first AIDS-1 patients were indeed typically users of “recreational” drugs p. 191 ff. in 16, pursuing a “fast-lane” lifestyle p. 79 ff. in 17,99,100,p. 292 ff. in 894,895,896 conducive to ill health. They were on average in their mid-to-late thirties with histories of many bouts of syphilis, gonorrhea, and other infections 95,96,97,98. Centers for Disease Control & Prevention used a unique, bizarre, misleading statistical classification scheme that obfuscated the fact that drug abuse was the primary common feature among victims of AIDS chapter 1 in 16.“AIDS” was a new social phenomenon, irrational exuberance by a proportion of gay men following “liberation”, expressed in an impossibly unhealthy lifestyle pp. 119-20 in 5,99,100,101,102. It had first been designated more correctly as GRID: Gay-Related Immune Deficiency; though since it was only a small proportion of gay men who practiced the “fast-lane” lifestyle, most correct would have been FLLRID.

2.1.2The first AIDS-1 patients had not been in sexual contact with one another 103. AIDS-1 came to be regarded as infectious only after the mistaken conclusion that HIV causes AIDS.

2.2Following the mistaken identification of “HIV” as cause of AIDS-1, an increasing number of diseases have come to be labeled “AIDS” just because in their presence an “HIV” test is fairly often positive. That defines AIDS-2: “HIV-positive” by definition, as in the now-common usage “HIV/AIDS”, which masks the fact that AIDS-1 was not HIV-caused. Recently the term “HIV disease” has become common.

By subliminal definition creep, “HIV disease” has come to include dozens of ailments, many of which are not opportunistic infections and all of which are previously known conditions, for example tuberculosis, weight loss or wasting, dementia 104.

2.2.11985 definition (AIDS-2a): “HIV-positive” and additional opportunistic infections beyond KS, PCP, or candidiasis 105.

2.2.21986 definition (AIDS-2b): “HIV-positive” and low CD4 counts and opportunistic infections 105.

2.2.31987 definition (AIDS-2c): “HIV-positive” “[r]egardless of the presence of other causes of immunodeficiency” [emphasis in original] and in presence of more than a dozen diseases 106.

2.2.41993 definition (AIDS-2d): Re-definition increased number of “AIDS” cases in that year by 75% 107.

2.3AIDS in Africa (henceforth AIDS-Africa) is neither AIDS-1 nor AIDS-2 108.

2.3.1Although AIDS-2 had been defined as caused by HIV, the lack of HIV-testing facilities in Africa led to defining AIDS via the Bangui definition 109: chronic or persistent weight loss, diarrhea, fever — entirely non-specific symptoms consistent with any number of endemic African diseases. dying from “AIDS” are succumbing to diseases that have ravaged Africans for centuries 108,110. the criterion for AIDS diagnosis in Africa is independent of “HIV”, one cannot know how many African “AIDS” patients are HIV-negative 32. Malnutrition is widespread in Africa and is a known cause of lack of resistance to infection. It can be responsible for any infection incurred within 1 month of the end of food deprivation 870.


3.1“HIV tests” have never been shown to detect “HIV”, namely an exogenous retrovirus 111,112,113,114,115,116. Therefore the term HIV denotes only whatever it is that produces a positive HIV test, and this should be indicated by always writing “HIV” or F(HIV) chapter 9 in 5 or something similar.

3.1.1That a retrovirus could be found in AIDS patients had been inferred from the presence of reverse transcriptase 117,p. 1259 in 118, an enzyme used by retroviruses to infiltrate the DNA genomes of the cells they invade. But reverse transcriptase turned out to be present in all mammalian cells and is not a valid marker for the presence of “HIV” 119 or any other retrovirus.

3.1.2The mistaken claim to have found a retrovirus in AIDS patients became a claim, announced at a press conference 120, that it was the probable 121,122,123 cause of AIDS, discovered by Robert Gallo. The articles later published by Gallo 49,124,125,126 did not establish that claim (see section 1.2.1).

3.1.3“HIV” tests have never been validated against a gold standard 127,910, namely, authentic pure virions (virus particles). virions of “HIV” have never been isolated from an AIDS-1 patient nor from an “HIV-positive” individual 50,111,128,129,130,131.“Isolation of HIV” in the mainstream HIV/AIDS literature does not carry the usual meaning of isolation, namely, separating out and purifying; instead, the so-called “isolation” of HIV involves a complex culturing technique without subsequent purification; it amounts to a self-fulfilling prophecy 132. only published electron micrographs of “isolated” “HIV” show a motley mixture of particles and debris that may not even include any retrovirus particles pp. 127-9 in 119,129,133. reward of $100,000 for an electron micrograph of isolated pure HIV virions was offered in 2002 and has never been claimed 134. has acknowledged that his laboratory never isolated pure HIV 135,136,137. acknowledged that his laboratory had not isolated HIV; he even claimed that copious production of HIV in culture was superior to isolation and purification and that it had made purification unnecessary pp. 1257-8 in 118. “HIV”, a “molecular clone”, contained only between 1 in 10,000 and 1 in 10 million actually infective virions and they were unstable, self-destructing quickly 138. Various sources make available "HIV-1 isolates". These should not be confused with authentic pure HIV particles (virions), which have never been prepared. The National Institutes of Health list 901 an "International panel of 60 HIV-1 isolates". Penn Center for AIDS Research lists 11 "Prototype HIV-1 Strains" 902 and 66 "Primary HIV-1 isolates" 903 as well as 9 "HIV-1 mutant viruses" 904. This variety already suggests that there is really no such thing as an "HIV virus". These so-called "HIV-1 isolates" are mixtures of a variety of different particles (vesicles) and different substances misinterpreted as "rapidly evolving quasispecies [of HIV]" 905 or "a complex mixture, or swarm, of mutant virus variants" 906.

3.1.4“Validation” of “HIV” tests is a self-fulfilling tautology 139,140,141.

3.1.5The instructions in test kits acknowledge that the tests are not approved for detecting infection 142,143.

3.1.6The first “HIV” test — “ELISA” (enzyme-linked immunosorbent assay) — detects antibodies 144,145 that are presumed to characterize “HIV” proteins, but these and later tests react “positive” to many kinds of antibodies, other proteins, or bits of RNA or DNA. “HIV” tests are not specific, see section 3.2. the tests detect active virus infections came to be believed without the benefit of evidence 146. belief, that detection of antibodies demonstrates presence of active virus, is an unprecedented and unwarranted inference: antibodies indicate earlier exposure, not infection, and in absence of manifest symptoms of illness antibodies are regarded — except only with HIV — as a priori evidence of established immunity to the respective infection.

3.1.7Measurement by PCR of so-called “viral load” (the purported amount of HIV particles in “HIV-positive” individuals) has been criticized as inherently invalid by the inventor of PCR, Nobelist Kary Mullis 147.“Viral load” measurements may not be specific to the presumed “HIV” genome 148.“Viral load” measurements yield appreciable numbers of false negatives 149.“Viral load” measurements yield appreciable numbers of false positives 149,150.“Viral load” measurements suffer from poor reproducibility 149,151,152.“Viral load” is not a marker for risk of death or progression to disease 153,154,155.“Viral load” does not measure amount of virus, since virus could not be cultured from some people with significant “viral loads” 156,157.“Viral” genes can be found in “HIV-negative” individuals 158,159,160,161.

3.1.8There are no valid “confirmatory” tests. Although Western Blot is routinely referred to in that way, its criteria have never been standardized or validated 127,162,163,164 and it is itself also liable to false positives 165.

3.1.9The initial “HIV” test was based on blood drawn from gay men who were manifestly ill “with AIDS”. No surprise, then, that a wide range of illnesses or degrees of ill health conduce to testing “HIV-positive”: for example, TB patients and drug addicts are as likely to test “HIV-positive” as are gay men, who were the very first purported “risk” group for “AIDS” 166.

3.2False-positive “HIV” tests are common 165,167,168,169,170,171,172,173. For consequent misinterpretations and their consequences, see sections 4.3 & 6.1 respectively.

3.2.1Rates of false-positive “HIV” test-results depend on the prevalence of positive-testing substances in the tested population. At the prevalence of “HIV-positive” (<1%) typical in populations outside southern Africa, the rate of false positives is likely to be quite high 127.

3.2.2Dozens of physiological conditions — normal, in disease, or owing to medical treatment — conduce to false-positive “HIV” tests 110,145,175,176,177,178,179 — possibly because “HIV-positive” correlates with oxidative stress 180,181,182,183,184,185,186 (more about oxidative stress in sections,,,,, Auto-Immune Diseases and antibodies to many stimuli 187,188,189,190,191,192,193,194,195,196,197,198,199,200,201; anti-carbohydrate antibodies 178,202,203; anti-collagen 204; anti- lymphocyte 204,205; anti-phospholipid (“sticky blood”) 80,206; HLA antibodies 178,179,187,188,189,197,207,208,209,210; mother’s antibodies transferred to babies 211; normally occurring antibodies 203,212,213; antibodies to components of test kits 196,214; lupus 215,216. that are not infectious: Cancers (cervical cancer 217,218); cardiovascular, atherosclerosis 219,220; chronic obstructive pulmonary disease (COPD) 221; cutaneous T-cell lymphoma 232; cystic fibrosis 222,231; diabetes 197; hemophilia 187,188,913; kidney failure and dialysis treatment 178,179,187,188,205,216,223,224,225,226,227,228; leprosy 229,230; multiple myeloma 187,189,210; multiple sclerosis 231,232; periodontal disease233; rheumatoid arthritis 238; genital inflammation 919,920. and toxins: Aflatoxin 234; cytomegalovirus infection 235; Epstein-Barr virus 236,237; flu (and flu vaccination) 178,189,238,239,240,241,242,243,244,245,250; hepatitis 179,187,188,210,225,246,247,248; herpes 249,250,251,252,253,254,255,256,258; HTLV p. 248 in 257; malaria 258,259,260,261,262,263,264,265,274,266; Mycobacterium avium 230; paramyxovirus 199; schistosoma 267; syphilis 179,187,188,197,268,269,287,320; Trichomonas vaginalis parasites 270,271; Trypanosoma parasites (Chagas disease) 272,273,274; tuberculosis 230,258,275,276; visceral leishmaniasis 277,278. procedures: Blood transfusion 178,188,189,209,24,238,279; globulins, in sick people or given as prophylaxis 110,178,189,262,280,281,282.283,284,285,286,287; hormonal contraception 288,289,290; organ transplants 178,179,205,238,291,292,293. conditions, not unhealthy: Pregnancy Fig. 22 p. 83 in 5,178,189,210,238,294,295,296,297,298,299,300,301,302,303,304,305,874; receptive anal sex 111. components of human cells: HIV-like genetic sequences occur in HIV-negative human genomes 306,307,308 and can generate immune responses to “HIV” proteins 309,310,311; supposedly “HIV” proteins occur normally in many human cells 178,179,172,313,111,315; normal human extravillous trophoblast cells express “HIV-1” antigens 316.“Recreational” drugs: 231 Alcohol 317; cocaine 317; crack cocaine 317,318; crystal meth 319; methamphetamine 320. Experimental HIV vaccines 321; flu 322 (also see above under infections); globulins (also see above under medical procedures); hepatitis B vaccination 189,323,324; rabies 190; rubella 325; tetanus 326,327,328. Fever is very non-specific. “HIV-positive” is often associated with fever 874.

3.2.3False positives are especially common in emergency rooms since the probability of a positive “HIV” test increases with degree of ill-health Fig. 22, p. 83 in 5, and associated text. Cincinnati with a population “HIV-positive” rate of 1.7 (per 100,000), the emergency-room rate was 7.8 329. 9 of 26 “HIV-positive” test results in an emergency room were positive on a later test 329.

3.3HIV — rather “HIV-positive” — has never been shown to be infectious or transmissible.

3.3.1Prospective studies to detect sexual transmission of “HIV” seropositivity have not observed transmission 330,331. In Africa, more than two thirds of couples are serodiscordant: one is “HIV-positive”, the other is not page 118 in 875.

3.3.2The often-cited rates of transmission are calculated by making unprovable assumptions, including about when individuals became “HIV-positive” 330.

3.3.3 The Centers for Disease Control & Prevention report the probability of transmitting HIV from female to male by vaginal intercourse as 4 in 10,000; from male to female, 8 per 10,000; by receptive anal intercourse, 138 in 10,000; by insertive anal intercourse, 11 in 10,000. Those numbers are far too low to bring about any sort of epidemic; (see section 3.3.12). With genuinely sexually transmitted diseases — gonorrhea, syphilis, herpes — the probability of transmission is hundreds of times greater 918.

3.3.4Mother-to-child transmission has not been shown to occur. transferred are substances that produce positive “HIV” tests, in particular “HIV” antibodies. Those dissipate within a year and “HIV-positive” babies then revert to “HIV”- negative without medication Fig. 2 and Tables 25-27 in 5,332.“[T]here is no proof that HIV, even if it is assumed to be present in pregnant women, is perinatally transmitted to their offspring” 333. presently available data do not prove that HIV can be transmitted by breastfeeding 333. Babies breast-fed exclusively by “HIV-positive” mothers become “HIV-positive” less frequently than those not fed solely from the breast 334,335,336. The research about mortality and “HIV” transmission associated with breast-feeding has brought inconsistent and confusing results 337,338. large percentage of “HIV-positive” babies had “HIV”-negative mothers 339,340.

3.3.5“HIV” varies in regular fashion and independently with age, sex, race, and geography, unlike the stochastic patterns seen in infectious diseases 5,341,342 — see also section 3.4 below. median age-range for testing “HIV-positive” is 35-45 Fig. 2, p. 26 in 5, comparable to the median age-range for diagnoses of AIDS and for deaths from AIDS 343,344,345,346,347. These have remained unchanged throughout the AIDS era and are the same in almost every tested group.

3.3.6The Office of Medical and Scientific Justice has successfully defended dozens of “HIV-positive” people (52nd case in June 2013) charged with endangering others by exposing them to possible transmission of “HIV”: OMSJ forces the prosecution to acknowledge — at least implicitly by altering charges or dropping prosecutions — that positive “HIV” tests do not prove infection 348.

3.3.7Innumerable attempts to create a vaccine against “HIV” infection have all failed 349,350,351,352,353 during the nearly 3 decades since Robert Gallo in 1984 envisaged a vaccine being ready within a couple of years 354,355,356, despite continuing pronouncements of optimism and announcements of promising “breakthroughs” 357.

3.3.8Drug addicts supposedly become “HIV-positive” through re-use of infected needles, yet use of fresh new needles increases rather than decreases the incidence of “HIV-positive” tests 358,359,912. rehabilitated drug addicts can revert from “HIV-positive” to “HIV”-negative 360. was little difference in risk behaviors between HIV-negative and HIV-positive drug- injecting gay men 361. use and venereal disease but not sexual behavior were risk factors for being “HIV-positive” among gay men 362. That the drugs are responsible for high rates of "HIV-positive" among drug abusers, and not infection via pre-used needles, is demonstrated by the very small probability of transmitting "HIV" via needles: 63 in 10,000 by sharing needles when injecting drugs, 23 per 10,000 by needle-stick in the skin 918.

3.3.9Medical personnel are extraordinarily unlikely to be infected by “HIV” or “AIDS” whereas they run appreciable risk with hepatitis, for example 88. An “HIV-positive” surgeon performed many open-heart surgeries without any patient becoming “HIV-positive” 364. “There is no recorded case of transmission of HIV from an infected health care worker to a patient in the UK [as of November 2006]” 365.

3.3.10Condoms do not decrease the incidence of “HIV-positive” 366,367,368.

3.3.11HIV and AIDS are almost unknown in the porn industry 369,370,371 even though chlamydia and gonorrhea infection and re-infection are common 372.

3.3.12The claimed rate of “HIV-positive” in sub-Saharan Africa can only be explained by postulating an impossible rate of promiscuity: 20-40% of adults having 10 or more sexual partners at any one time and changing them frequently pp. 63-5 in 373.

3.3.13Thus there are no demonstrated epidemics of heterosexually transmitted “HIV” 374.

3.3.14Racial disparities in prevalence of “HIV-positive” do not correlate with respective sexual behavior 375,376 and thereby seem inexplicable on HIV/AIDS theory.

3.3.15The incidence of “HIV” does not parallel the incidence of known STDs (chlamydia, gonorrhea, syphilis) pp. 35 & 109 in 5,377,378,893.

3.3.16Married women are more at risk for becoming “HIV-positive” than are prostitutes or widows, incongruous for any sexually transmitted disease 379,380.

3.3.17That pregnancy is a risk factor for testing “HIV-positive” (section is incongruous for any sexually transmitted disease.

3.3.18Prostitutes do not become “HIV-positive” unless they are drug addicts 12,pp. 41-2 in 20,381,382,465.

3.3.19Drug addicts tend to test “HIV-positive” to different degrees from different drugs 360.

3.4“HIV” tests are racially biased.

3.4.1In any group, black people (people of relatively recent sub-Saharan ancestry) test “HIV-positive” about 7 times (males) or 20 times (females) more often than Caucasians. Asians test “HIV-positive” about 2/3 as often as Caucasians. Native Americans and Mexicans test “HIV-positive” perhaps 10-20% more frequently than Caucasians chapters 5 & 6 & passim in 5,383,384,385. supposedly “HIV” protein p24 generates a stronger response in black people than in others 386. levels of “HIV-1 RNA” were found in Malawians than in Swiss or USA men 387. and Caucasians differ genetically with respect to the human T-cell antigen receptor 388.


HIV/AIDS theory has persistently led to wrong predictions and to inadequate or totally missing, and not infrequently absurd, explanations. After three decades, basic issues remain unresolved about isolation and identification of "HIV", about epidemiology, and about anti-retroviral drugs 911.

4.1Predictions have invariably been wrong.

4.1.1“Generalized” epidemics leading to “HIV-positive” population levels of more than 1% have never eventuated outside populations of African ancestry, namely sub-Saharan Africa and the Caribbean 389.

4.1.2Even in sub-Saharan Africa, “HIV-positive” levels are “explained” by postulating an impossible level of promiscuity pp. 63-5 in 373 (see also sections 3.3.12 & 6.1.4).

4.1.3Predicted Philippines epidemic did not happen 390.

4.1.4Forewarned epidemic in porn industry 391 never eventuated despite lack of condom use.

4.1.5Predicted Asian epidemics never eventuated 392. In 1995, Peter Godwin, head of the Regional HIV Project, United Nations Development Program: “by the year 1997 the annual number of new HIV infections in Asia will exceed those in Africa, and its share of worldwide cumulative infections will increase to nearly 25% by the year 2000” 876 but by 2007, Asia had only 5 out of a global 33 million “HIV-positives” while sub-Saharan Africa had 19 million 875.

4.1.6Predicted decimation of populations did not occur in Africa. Instead, there has been robust population growth 110: “Recent [2007] reports from Uganda, Kenya and Burkina Faso show . . . concern over rapid population growth” 393.

4.1.7Vaccines were predicted within a couple of years of 1985 and have never been achieved 357.

4.1.8“Breakthroughs” in preventing or treating infection are announced — and then never live up to their promise 394,395,396,397,398,399,400,401,402,403,404,405,406,407,408,409,410,411,412,413,414,415,416,417,418,419. Horse inhibitors 877,878,879. Killing “HIV” by shaking it with tuned laser 880.

4.2Public statements emphasize how much is known about HIV/AIDS, yet researchers do not understand many practical as well as theoretical aspects.

4.2.1“We probably know more about how HIV produces its pathology than about the pathological mechanism of virtually any other microbe” 420.

4.2.2“[I]dentification of immune correlates of protection from HIV infection is still lacking” 421. In other words, no clue (by 2013!) about how to make a vaccine.

4.2.3“35 top British and US scientists . . . predicted this week [29 April 2008] that a vaccine would be at least 10 years and maybe even 20 years away” 422 (see also sections, 3.3.7, 4.1.7).

4.2.4The recommended treatments are revised several times a year (section 5.4), including when to begin treatment 421.

4.2.5Characteristics of the purported “acute viral syndrome” postulated to accompany initial infection — sometimes — are speculative: “diagnosis of acute HIV-1 infection remains problematic” 423. manifest signs accompanying infection by “HIV”, a correlation has sometimes (e.g. in 20% of cases 424) been suggested with transient “flu-like” or mononucleosis-like 425,426 symptoms that are entirely non-specific 427: fevers, sweats, malaise, lethargy, anorexia, nausea, myalgia, arthralgia, headaches, sore throat, diarrhoea, generalised lymphadenopathy, rash 428 (sometimes “macular erythematous truncal eruption”), thrombocytopenia. Since those symptoms as well as “HIV-positive” can result from a large number of different conditions, fleeting as well as chronic, the phenomenon of “acute viral syndrome” cannot be regarded as established. symptoms could only be potentially connected to “HIV” or “AIDS” by some sort of prior assumption, which makes the purported correlation a self-fulfilling presumption. Why were such symptoms not only noticed but also suspected of being associated with “HIV” rather than with flu, mononucleosis, or the many other possibilities? So “[d]iagnosis of primary HIV infection remains a relatively infrequent occurrence [in 2008]” 429, and generalizations currently accepted may well be mistaken. is assumed that such symptoms indicate high levels of viremia 430 — but since “HIV” tests are generally not carried out concurrently with the “acute viral syndrome” 431, this is mere presumption. postulate of “acute viral syndrome” with HIV/AIDS was made already in the early 1980s 432 and has subsisted by inertia without serious reconsideration.“Clinical signs and symptoms of acute human immunodeficiency virus (HIV) infection in infants are not well characterized” 433.

4.2.6How “HIV” could damage the immune system remains a mystery 434,435,436,437,864,881.

4.2.7When and how HIV appeared in humans remains controversial 438.

4.3Treatment of “HIV-positive” individuals and HIV/AIDS research are misguided through misinterpretation of positive “HIV” tests.

4.3.1Genetic, race-correlated tendencies to test “HIV-positive” are misinterpreted. genes are postulated to drive mutation of HIV 439.

4.3.2Conditions that conduce to positive “HIV” tests are misinterpreted as susceptibility to “HIV” infection; see the list of false-positive possibilities, section 3.2. unhealthy “fast-lane” lifestyle (drug abuse, alcohol abuse, promiscuity with frequent infections and courses of antibiotics) conduces to testing “HIV-positive”. addicts who test “HIV-positive” are presumed to have been infected with “HIV”. to gut bacteria and mucosa (intestinal dysbiosis) is attributed to “HIV” 437,440,441 whereas strong evidence indicates the opposite, that testing “HIV-positive” is a result of damage to the gut (see sections, 9.3.1). Probiotics increase CD4 counts 442.“AIDS” may reflect oxidative stress rather than a viral infection 80 (see also sections, 3.2.2,,,, but “HIV” is held responsible for causing oxidative stress 454. several Central Asian countries, inexplicable cases of “HIV-positive” are ascribed to infection in some unknown manner by needles supposedly infected from some unknown source instead of to birth stress and other conditions that can produce positive “HIV” tests 443,444. treatment against bacterial vaginosis is misinterpreted as acting against “HIV” 445,446. who test “HIV-positive” are assumed to have been infected by blood transfusion or blood-clotting factor 447,Appendix A in 10,passim in 20,913. problems are attributed to “HIV” 448,449 instead of realizing that stress, including psychological stress, can induce testing “HIV-positive” Fig. 22 & p. 80 ff. in 5 (re oxidative stress, see sections, 3.2.2,,,, aneurisms are attributed to “HIV” 450,451. Cardiovascular disease 882.

4.3.4Iatrogenic ailments caused by ARVs are legion (section 5.3), but they are often misattributed as “HIV-associated”:, which is caused by protease inhibitors in particular 452.“HIV-associated” arthritis, said to include reactive arthritis, psoriatic arthritis, osteomyelitis, polymyositis, vasculitis, infected joints and fibromyalgia 453. conditions (cancer. dementia, heart disease) 454.“HIV-associated” mania 455,456,457. attacks 458,459. 460,461,462. disease 463. Bone disease, osteopenia, osteoporosis 883.

4.3.5Three decades of efforts to find a vaccine against “HIV” have failed (sections 3.3.7, 4.1.7, 4.1.8, 4.2.2, 4.2.3) even though quite a number of people with natural immunity against “HIV” have been identified and studied 464,465,466,467,468,469,470,471,472,473,474,475,476.

4.3.6Decades of efforts to find a microbicide have also failed 477,478,479,480.“The trial did not demonstrate that Carraguard is effective in preventing male-to-female HIV transmission” 481.

4.4A number of basic aspects of HIV/AIDS theory are known to be wrong.

4.4.1The so-called “latent period” between infection and illness, an essential component of the original labeling of HIV as a lentivirus (slow virus), doesn’t exist 482,483.

4.4.2KS was the iconic AIDS disease, recognized by the purple blotches on the skin and affecting 25-40% of AIDS patients in the early 1980s. But since the early 1990s 484 and thereafter only about 5% of AIDS cases have manifested KS. Furthermore, Kaposi’s sarcoma is now said to be caused primarily pp. 125-9 in 5,485,486,487 by HHV-8 (human herpes virus 8) or KSHV (Kaposi’s sarcoma herpes virus) — and “HIV-associated” KS may not even be a cancer 488.

4.4.3Cervical cancer had been declared to be an AIDS disease 489, i.e. caused by “HIV”, but now it is said to be caused by HPV, human papilloma virus 490. is a mystery, why cervical cancer was ever declared an AIDS disease, given that its incidence had been declining steadily throughout the AIDS era 490,491.

4.4.4HIV is supposed to kill CD4 cells, but there is no correlation between CD4 levels and the purported amount of “HIV” (“viral load”) or even the patient’s clinical condition 154,493,494,495,496. There is no correlation between CD4 counts and state of health 897.

4.4.5“HIV-positive” is not permanent; people sometimes spontaneously become “HIV-negative”, a phenomenon known as seroreversion 497,498,499,500,501,502.

4.4.6Low T-cell counts are a predictor for becoming “HIV-positive”, they are not a consequence of “HIV” 503,504.

4.4.7The theoretical basis for Highly Active AntiRetroviral Treatment, HAART, was that there was very rapid turnover of T-cells 505,506. That model has been shown to be wrong 507,508,509,510.

4.5HIV/AIDS statistics are unreliable 511,512.

4.5.1UNAIDS 513 inflates estimates in order to dramatize the situation 373.

4.5.2For more than a decade, official data for “HIV” and “AIDS” have come from computer models and not actual counts pp. 114 & 135-6 & 203-10 & 221-5 in 5,515,516.

4.5.3The computer models have needed perpetual correction 517,518; for example, estimates of new infections were reduced by 40% in 2007, and totals reduced from 40 million to 33 million 519.

4.5.4Estimates of deaths by the Division of HIV/AIDS of the Centers for Disease Control and Prevention (CDC) differ from the counts of death certificates by the CDC’s own Center for Health Statistics 520,521,522.

4.5.5Peer-reviewed , published, and widely publicized assertions about AIDS deaths in South Africa 523,524,525 are based on computer models whose estimates are more than on order of magnitude greater than the published data from South Africa Statistics 74.

4.5.6The World Health Organization claimed 85,000 “HIV-positive” Pakistanis when only 3200 were actually known from tests 527.

4.5.7HIV/AIDS numbers asserted for Liberia during the 2000s varied between 1.5% and 8.2% 528.

4.5.8Circumcision is reported as both decreasing the risk of becoming “HIV-positive” and as not decreasing the risk 529,530,531,532,533,534, 535,536,537,538,539,540,541,542,543,544. increased the rate of “HIV-positive” among virgins 545.

4.5.9Absurd numbers are promulgated (sections 4.7.16, 4.7.18). claimed reduction in “HIV-positive” rate from 34% to 18.1% between 2002 and 2005-6 — implying that 15.9% of the population had died in five years if there were no new “HIV-positive” cases, or else the population had grown at 3% per year with no new infections 546,547. Or the rate was said to have dropped from 22.1% to 20.1% in just two months 548. absurd claims have come from Uganda 304,549.

4.6The origin and spread of HIV have found no satisfactory explanation.

4.6.1AIDS was first named and recognized as characteristically affecting gay men in a few large cities in the United States, but HIV is held to have infected humans for the first time in West Africa at least a decade earlier and perhaps several decades earlier 14,550. 1985, “HIV” in Southern Africa was found only in gay men who had been in the USA or in contact with Americans 551,552. was the chief opportunistic infection characterizing the original AIDS-1. In AIDS-Africa it apparently affected only young children 553,554.

4.7Self-contradictions and absurdities of HIV/AIDS theory and practice.

4.7.1That pregnancy (section, 3.3.17, is a risk factor for acquiring this sexually transmitted disease.

4.7.2HIV/AIDS activists insist that no stigma should be attached to those who become “HIV-positive” even as HIV/AIDS theory asserts that “HIV” is contracted through behavior that is appropriately frowned upon: careless promiscuity or drug abuse and injecting drugs with dirty needles.

4.7.3HIV/AIDS activists urge that drug abusers be given new needles so that they can “safely” inject heroin and other “recreational” drugs. In every circumstance except HIV/AIDS, use of illegal injected drugs is regarded as criminal behavior 555,556, and it is recognized that drug addicts harm their families as well as themselves. Moreover, clean needles are associated with greater incidence of “HIV-positive” (section 3.3.8), owing to the ill-health brought about by the drugs.

4.7.4“HIV” is supposed to spread by different mechanisms in different parts of the world 557,558,559.

4.7.5Those who are most susceptible to becoming “HIV-positive” nevertheless live longer 560.

4.7.6Poverty is supposed to conduce to “HIV-positive” by increasing risk factors, but in Africa it is wealth that conduces to being “HIV-positive” 561,page 89 in 875.

4.7.7An “HIV-positive” man who did not infect his wife despite intercourse with her must have nevertheless infected his child by biting her finger 562.

4.7.8Babies infected by dirty needles are supposed to have transmitted “HIV” to their mothers by biting their nipples 563.

4.7.9Breast-feeding by “HIV-positive” mothers is said to risk transmitting HIV to the babies, yet exclusive breast-feeding brings the lowest risk that babies will become “HIV-positive” 334 (section

4.7.10Tuberculosis (TB) patients test positive as often as do gay men and drug addicts Fig. 22 p. 83 in 5,564 so, irrationally, TB is sometimes said to be an AIDS disease rather than just TB.

4.7.11Cervical cancer was said to be an “AIDS disease”, i.e. caused by “HIV”, in 1993 489. Yet nowadays it is said to be caused by human papillomavirus (HPV), again on the basis of a mere correlation.

4.7.12Increased obesity is attributed to desire to show that one is not “HIV-positive” 565.

4.7.13When malnourished Africans test “HIV-positive”, their ill-health is attributed to “HIV” rather than lack of food 110,566.

4.7.14“Washing the penis minutes after sex increased the risk of acquiring H.I.V. in uncircumcised men. The sooner the washing, the greater the risk of becoming infected” 567.

4.7.15When ARVs appeared to work against “HIV” but patients nevertheless became more ill, this was ascribed to the newly invented “immune restoration syndrome”: recovery or re-activation of the immune system supposedly caused inflammation and illness 568,312.

4.7.16Official numbers just don’t compute 569. Estimates have perhaps one in four 570of “HIV-positive” Americans unaware of their status — up to 75% of gay men 571, even 93% of young gay black men 572 (and about a third of “HIV-positive” people in Britain 573,574). Now, about 1 million Americans have been “HIV-positive” throughout 3 decades pp. 1-2 in 5. By 2 decades ago, therefore, assuming the 10-year “latent period” (which doesn’t actually exist 482,483), at least 250,000 “HIV-positive” people should have been coming down with AIDS and dying within a year or two, being replaced by the ~55,000 new annual infections 575 to somehow keep the total number of infected at about 1 million. But reported HIV/AIDS deaths rose to a peak of 42,000 in 1994 and then declined steadily to <16,000 576.

4.7.17 Measles virus slows progression of HIV infection 577,578,579,580,581.

4.7.18 “HIV” tests are sometimes said to be 100% sensitive and 100% specific 582.

4.7.19 Sleeplessness and not taking ARVs are correlated [big surprise] 583.

5. WHAT ANTIRETROVIRAL DRUGS DO 584,585,586,587,588

The criterion for effectiveness of ARVs is action in reducing “HIV-positive” or “viral load” or increasing CD4 counts, judged initially by in vitro experiments. But this does not necessarily correlate with clinical improvement of the patient 154. This is a real-life illustration of the old saw that an operation may be judged by the experts to have been successful even if the patient died. Suppression of "viral load" does not always restore the immune system 917; level of "viral load" does not correlate with level of CD4 cells and neither correlates with clinical condition of the "patient" 154.

5.1 There is no evidence that ARVs prolong life 68,589,590 or improve the quality of life 591,592,593,594,595,596,597.

5.1.1Despite FDA warnings, manufacturers advertise ARVs misleadingly as though they allow a completely healthy life 598,599,600. Some people become manifestly more ill as soon as they start taking ARVs. This happens so often that it has been given a name, "immune restoration syndrome" 312.

5.1.2“Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality” 601. of 25-year-old “HIV-positive” people responding successfully to HAART was 5.3 and 10.4 times greater than in the general population, for men and women respectively 602.

5.1.3No life-prolonging benefit is claimed for AZT in a review that attempts to calculate the supposed benefits of ARVs 603.

5.1.4Deaths from “AIDS” continued to increase after the introduction of AZT treatment. The proportion of AIDS patients surviving for even one year was not increased by AZT plus prophylaxis against PCP 604.

5.1.5AZT actually killed about 150,000 “HIV-positive” people between the mid-1980s and the mid- 1990s 68. effects unpleasant enough to report were experienced by 50-75% of healthy medical personnel treated for possible exposure to HIV, and the side effects were severe enough that 24-36% discontinued the therapy 605.

5.1.6When AZT was replaced by “cocktails” [Highly Active AntiRetroviral Treatment (HAART) or Combination AntiRetroviral Therapy (CART)] the death rate of “AIDS” patients almost instantly declined solely because the new treatment was less toxic 68,604.

5.2The very concept of ARVs was misguided.

5.2.1Bacterial and parasitic infections can be successfully treated with antibiotics because those can kill bacteria and parasites without killing the human patient: the physiology of the invading agents is sufficiently different from that of the patient. By contrast, viruses use the host’s biochemical machinery, so preventing virus replication means disabling some of the body’s essential mechanisms.

5.2.2Nevertheless, social hysteria over the putatively fatal, sexually transmitted “HIV” led to a trial- and-error search for virus-killers.

5.2.3The initial clinical trial of AZT 606,607 — interpreted as showing that AZT extended by a few months the lives of AIDS-1 patients who were at death’s door — was badly flawed 608,609, as was 610 the later, much larger “Concorde” trial 611.

5.2.4AZT (Retrovir), renamed zidovudine (ZDV), is a nucleoside reverse transcriptase inhibitor (NRTI). Nowadays it is acknowledged that these drugs are not effective “HIV”-killers: “Single-NRTI therapy does not demonstrate potent and sustained antiviral activity and should not be used (AII). For prevention of mother-to-child transmission (PMTCT), zidovudine (ZDV) monotherapy is not recommended but might be considered in certain unusual circumstances . . . .” [emphasis added] 612. AZT monotherapy for PMTCT had been introduced in 1994 and later, in the HAART era and until at least 2007, “[d]uring pregnancy, HIV-1-infected women in industrialized nations . . . commonly receive[d] highly active antiretroviral therapy . . . that generally consist[ed] of three or more drugs, including two . . . NRTIs . . . . most frequently. . . AZT and lamivudine [3TC]” 613.

5.2.5Mainstream data should have made it obvious long ago that AZT therapy is too carcinogenic 614 (section as well as toxic (in particular to mitochondria, sections 5.2.6,, to use in humans and moreover could not defeat “HIV” 615 (sections 5.1, 5.2.4).

5.2.6Nevertheless, NRTIs including AZT/ZDV remain a component of most combination therapies, despite lack of effectiveness and considerable toxicity: “ZDV can cause bone marrow suppression, myopathy, lipoatrophy, and rarely lactic acidosis with hepatic steatosis” 616; “Bone marrow suppression, manifested by macrocytic anemia and/or neutropenia, is seen in some patients. ZDV also is associated with GI [gastrointestinal] toxicity, fatigue, and possibly mitochondrial toxicity 613,617, including lactic acidosis/hepatic steatosis and lipoatrophy” 618. The manufacturer’s own pamphlet included a dozen pages detailing adverse reactions 619.

5.2.7Combination antiretroviral treatments are less obviously and speedily toxic than monotherapy because the dosages of each of the toxic substances are smaller and some of the components are somewhat less toxic than AZT.

5.3Toxic side-effects of ARVs are legion 620,621,622,623,624.

5.3.1"[A] growing proportion of patients receiving long-term antiretroviral therapy are experiencing treatment failure, drug toxicities, side effects, and drug resistance. . . . an increased incidence of malignancies, cardiovascular and metabolic complications, and premature aging associated with long-term HIV disease or antiretroviral therapy." 625

"Mortality of HIV+ hospital patients owing to non-AIDS events (non-AIDS infections, cancers, cardiovascular and liver diseases) was higher among patients receiving antiretroviral treatment." 921 of stavudine increased with dose and over time 626. December 2011, activists asked the Gates Foundation to cancel a clinical trial comparing stavudine to tenofovir because the former is so toxic 627. Risk of non-AIDS-related mortality may exceed risk of AIDS-related mortality among individuals enrolling into care with CD4+ counts greater than 200 cells/mm3 915. Liver fibrosis caused by some ARVs 916.

5.3.2The side-effects are so intolerable that patients’ non-adherence to treatment is a perpetual theme in the literature 628,629,630,631,632,633,634. Treatment Guidelines are replete with references to non-adherence 635, e.g. “Adverse effects have been reported with use of all antiretroviral (ARV) drugs; they are among the most common reasons for switching or discontinuing therapy and for medication nonadherence” 636.“Not surprisingly, nonadherence to prescribed medications is common in teens” 637.

5.3.3Specific side-effects impinge on every part of the body. prematurely 454,638,639; damage to mitochondria 613,617,640,641,642,643,644,645,646,647,649,650,651,690 could be a reason for this and for muscle deterioration 655 and oxidative stress 652 (re oxidative stress, see also sections, 3.2.2,,,, reactions including rash and skin death 653,654,655;, spontaneous, with all protease inhibitors 655. 613,656,657,658,659,660,661,662,663,664. nervous system effects 665,666 including psychosis 655,667: neuromuscular weakness, somnolence, insomnia, abnormal dreams, dizziness, impaired concentration, depression, suicidal ideation, depression 655. Functional and physiological disturbances: headaches 607; insomnia 607; Gallstones, apparently inevitable with protease inhibitors: “Median time to onset is 42 months (range 1–90 months)” 655. vomiting, nausea, diarrhea 607,655,668,669. syndrome 670,678 and metabolic dysfunctions 671: diabetes, insulin resistance 655,672,673,674,675,676,677,678,679,680; dyslipidemia (dysfunctional blood lipids) 655,672,674,675,676,677,678,680,681,682,683,684,685; lactic acidosis 655 ; lipodystrophy 655,672,674,675,676,677,678,680,683,684,686,687,688,689,690,691,692,693,694,695. deterioration and failure: anemia and bone-marrow suppression 607,655; heart disease including heart attacks 655,673,678,696,697,698,699,700,701,702,703,704,705,706,869; kidney disease, kidney stones 655,707,708,709,710; liver damage 655,711,712,713,714,715,716; neutropenia 717; pancreatitis 718; stroke 719. 655,720,721,885. stress 722 (see also sections, 3.2.2,,,, neuropathy 460,461,462,655. killing 607,723,922. Vitamin D deficiency 884.

5.4The official Treatment Guidelines 724 are perpetually revised, and once-recommended treatments become not recommended or to be avoided 725,726,727,728,729. Innumerable changes can be identified in successive versions of the Guidelines.

5.4.1Bear in mind that these revisions are based on knowledge gained through already observed severe damage in a significant number of cases (sections 5.1.5, 5.2.5, 5.3).

5.5Some physicians have successfully treated AIDS patients without resort to ARVs 730,731,732, though they sometimes resort to very short courses of ARVs, which are potent antimicrobials, to eliminate possibly occult bacterial infections.

5.5.1Juliane Sacher has had better success treating AIDS patients than other German physicians who use standard anti-“HIV” treatment 733,734,735.

5.5.2Claus Köhnlein has successfully treated AIDS patients without the anti-“HIV” approach 736.

5.5.3A decrease in opportunistic infections in “HIV-positive” individuals may not be due to killing “HIV” but to direct suppression of fungal infections 737,738.

5.5.4 "Lazarus Effect": Anecdotal reports describe "AIDS" patients on the point of death who recover immediately upon receiving antiretroviral drugs. But any antiretroviral action could only produce a very slow, lengthy effect. The Lazarus Effect demonstrates that antiretroviral drugs are very efficient killers of all cells, bacterial and mammalian, including the lymphocytes that produce inflammation 898,899.


6.1To individuals, through misinterpretation of positive “HIV” tests.

6.1.1Everyone who is ill for any reason is likely to be subjected to an “HIV” test and damaged (sections 6.1.2 and 6.1.3). greatest human tragedy of HIV/AIDS theory is that “HIV-positive” individuals who become ill for any reason at all — and sometimes who are not ill at all but tested “positive” because of a life-insurance examination or something similar — are classed as “having HIV/AIDS”. long as HIV/AIDS theory remains in force, there is a crying need for authoritative information for people who are told they “have HIV/AIDS”, many of them knowing with certainty that they could not have become infected in any of the ways that HIV/AIDS theory says they must have been. is a crying need for doctors to learn how to deal with laboratory results claiming “HIV-positive”: that none of the tests are approved for actually identifying infection; that there are any number of false positives; that there are no valid confirmatory tests; and that they should use every diagnostic tool available to determine whether there is any reason at all to think the person might actually have an illness. is a crying need for doctors to learn that a very common reason for an “HIV-positive” result is pregnancy (section is a crying need for doctors to learn that there are genetic, race-correlated factors that conduce to testing “HIV-positive” and that the tests are thereby severely racially biased pp. 100-2 & 171 in 5.

6.1.2Everyone who tests “HIV-positive” is thereby at risk of psychological and social harm. are not properly informed about the high probability of false-positive ”HIV” tests, particularly with low-risk individuals 739. is inferred with no further ado, and relationships are broken 740.“HIV-positive” individuals who engage in sex may be sent to prison for allegedly endangering their partners 741.“HIV-positive” individuals have been sent to prison even for spitting on someone 742,743,744.“Veteran who was WRONGLY treated as HIV positive for nine years sues hospital after being ‘emotionally and mentally destroyed’” 745. Tommy Morrison lost his career because of inconsistent “HIV” test-results 746.“HIV-positive” Asian women have been driven from their marital homes 747.“HIV-positive” women in Chile have been forcibly sterilized 748.

6.1.3 Everyone who tests “HIV-positive” is at risk of bodily harm from toxic (section 5.3) ARVs and from other experimental treatments. have been tested on foster children 749,750 and orphans 751,752,753,754 without proper safeguards. Chemotherapy to kill the immune system to avoid rejection of transplanted baboon bone-marrow cells because baboons couldn't be infected with "HIV" 886. The first attempt involved "an unidentified 56-year-old man who was dying of AIDS...The experiment was not a success. The baboon cells failed to grow, and the man died two months later. But Dr. Ricordi said his team had been encouraged because the man did not suffer any adverse reactions from the transplant" [emphasis added] 887,889.

6.1.4Black people are at particular risk because they test “HIV-positive” much more often than others; black women seem to be particularly at risk — see 3.4.1 ancestry is misinterpreted as behavioral risk of infection even though blacks test “HIV-positive” more often than others irrespective of behavior 755,756,757,758,759,760,761. promiscuous “concurrency” is postulated to explain the uniquely high sub- Saharan prevalence of “HIV-positive” 373,762,763,764 even though actually observed sexual behavior does not support the postulate of high levels of concurrency p. 78 in 5,375. people are presumed to be not only more promiscuous but also more likely to inject illegal drugs 765.“HIV-positive” black men are immediately assumed to be on “the down low” 766,767 — behavior that may be far less common than is now widely presumed 768,769.

6.1.5Gay men are at particular risk because something about the lifestyle seems to conduce to testing “HIV-positive”. only those gay men who practice the “fast-line” lifestyle, but data are lacking to reach firm conclusions. promiscuity is inferred from dubious data: “exactly the same strain of HIV can be shown to have infected all five of these people. . . . [and] transmission probably occurred from a single person to these various partners within just a few hours” [emphasis added] 770. Intestinal dysbiosis theory 735,771 suggests that deliberately responsible behavior like anal douching may actually conduce to becoming “HIV-positive” and even ill. Some "HIV-positive" gay men (as well as some women 907) occasionally suffer AIDS-like illness including low CD4-T-cell counts after having been healthy for as long as a couple of decades. Given that "HIV" does not cause immunedeficiency or AIDS, the circumstances of these people are mysterious in a way that is comparable 908 with those diagnosed as having "idiopathic CD4-T-cell lymphopenia" (section 1.1.5). Similar treatment might then be appropriate, namely, treating any manifest illnesses directly, preventing opportunistic infections, and strengthening immune systems, for instance with interleukin, interferon, or hematopoietic stem cell transplantation 909.

6.2To social institutions

6.2.1When finally it becomes universally recognized that HIV/AIDS theory is wrong, trust in the institutions of medicine and science will take a very severe blow.

6.2.2In the meantime, individual institutions may be sued for damages when positive “HIV” tests were mistakenly taken as proof of permanent “HIV-positive” status 745,772.

6.2.3Law enforcement gets egg on its face when prosecutions fail because they cannot prove the transmissibility of “HIV” 348,773.

6.3To society as a whole: Huge sums of money have been and continue to be wasted on anti-“HIV” and anti-“AIDS” activities.

6.3.1The United Nations HIV/AIDS program 774 and National Institutes of Health 775,776 spend disproportionate amounts on “HIV/AIDS” compared to other health concerns.

6.3.2In Africa, billions of dollars are spent on ARVs and associated activities when far smaller amounts could improve health and save lives immediately 110,777,778,779, for example by providing:
a. means for water purification;
b. minimal amounts of decent food 777;
c. treated anti-mosquito nets to prevent malaria;
d. $35 oxygen valves for hospitals 777.

6.3.3Billions of dollars continue to be spent on attempts to find an anti-“HIV” vaccine despite 3 decades of evidence that it cannot be done (sections 3.3.7, 4.1.7, 4.1.8, 4.2.2, 4.2.3, 4.3.5).

6.3.4Well-intentioned “education” programs reinforce the hegemony of HIV/AIDS theory. Bill and Melinda Gates Foundation actually paid for entertainment programs to present the mainstream viewpoint about HIV/AIDS 780.

6.4 Hegemony of HIV/AIDS theory and practices means that some central questions cannot be answered.

6.4.1 When "HIV-positive" individuals become ill, all too often the real cause of illness is not looked for.

6.4.2 When "HIV-positive" individuals using antiretroviral drugs die, no autopsy inquires into whether death may have been owing to the drugs 888,889.


One difficulty is the massive misunderstanding of science that makes it seemingly inconceivable that it could go so massively wrong for so long (section 8). In addition:

7.1Misinformation is ingrained in the public sphere, in the conventional wisdom, about the discovery of “HIV” and the histories of HIV and of AIDS 781.

7.1.1That AIDS-1 first appeared among “young, previously healthy, gay men”. In reality they were not particularly young (average age mid- to late 30s) and far from healthy 95, characterized primarily by heavy drug abuse and a “fast-lane” lifestyle rather than by being gay 16. In the earliest days of the "AIDS" era, the Centers for Disease Control, in a quest for increased funding, instituted a PR campaign asserting that everyone is at risk for HIV, even as they knew that AIDS was restricted to specific "risk groups" 900.

7.1.2“HIV” tests are taken as showing infection, and “confirmatory” tests (typically Western Blot) are taken as validating that. In reality, neither presumption is correct, there are no valid tests for infection (sections 3.1, 3.2) and so-called “confirmatory” Western Blot itself is liable to false-positives 165.

7.1.3Antiretroviral therapy is not “life-saving”, as it’s often described 589 (section 5.1). The false claim is sustained in part by attributing toxic side-effects of ARVs to “HIV” rather than to the drugs 782,783,784,785,786,787 (section 4.3.4). aging is attributed to ARVs keeping people alive longer and supposedly suffering long-term damage from “HIV”, when actually ARVs are known to damage mitochondria (sections 5.2.5, 5.2.6,, and damage to mitochondria happens to be a direct cause of aging 788,789,790,791,792,793.

7.1.4References in fiction and on television 794,795,796,797,798,799 reinforce the hegemony of HIV/AIDS theory. “HIV” is readily spread by sexual intercourse 800,801. one could be infected by “HIV”-tainted blood splashed into one’s eye 802. HIV can be transmitted by saliva on a baseball 803. AZT is a powerful ARV 804., Daniel Easterman correctly noted in 1990 805 that some individuals could overcome AIDS by making lifestyle changes, possibly reflecting the experience of Michael Callen 101. That an HIV-infected needle on a chair seat can be used to assassinate someone, death following in 5 months 862. That smoking crack cocaine avoids worrying "about needles and AIDS" 863. That getting a tattoo risks getting AIDS from an infected needle 865. That many hemophiliacs were infected by tainted blood products. "Two thirds of our hemophiliacs have received infected blood" 890.

7.2Fresh misinformation about “HIV” and AIDS continually enters and pervades the public sphere 806.

7.2.1“News” items incessantly reinforce mistaken views by reiterating “HIV/AIDS”; “HIV, the virus that causes AIDS”; “life-saving” ARVs; etc. media typically broadcast “breaking news” about science and medicine but fail to revisit the topic when the original claim turns out to need modification or complete withdrawal, which is the usual circumstance with the latest from the research front 807 — for example, 30 years of promises and promising breakthroughs toward an “HIV” vaccine without any genuine, perceptible progress (sections 3.3.7, 4.1.7, 4.1.8, 4.2.2, 4.2.3, 4.3.5). and non-governmental agencies continually urge the media to campaign for awareness of HIV/AIDS theory 808. The mistaken belief that “HIV” is transmitted sexually (see section 3.3 for disproof) is incessantly repeated, for example that prostitutes contract and spread "HIV" 891,892.

7.2.2It takes longer to demonstrate the errors in a claim than to make the mistaken assertion. flaws in any new mainstream claim about “HIV” and “AIDS” can only be explained once it is recognized that HIV/AIDS theory is wrong. example, “antiretroviral drugs can forestall long-term health risks of the disease and cut the risk of transmission by as much as 96 percent” 809.

To debunk that sentence requires presenting the copious but circumstantial proof that “HIV” entails no “long-term health risks”, as well as surveying the copious data on toxicity of ARVs, not to speak of demonstrating the faulty statistics underlying that “96%”: since the claimed transmissibility is already so low (section 3.3.3), the reported “96%” cut could only be observed in a clinical trial of immense proportions and duration. Everything based on “HIV” tests is likely to be wrong and should not be accepted at face value, but to make the case with any specific claim requires debunking the whole basis and edifice of HIV/AIDS theory.

7.3The dissenters from HIV/AIDS theory do not agree among themselves about how to discredit HIV/AIDS theory or about what the correct explanations are for “AIDS” and “HIV”.

In addition, it is notoriously difficult to prove a negative case, and the case against HIV is in some sense a negative case. Science does not abandon an hypothesis just because it has flaws and cannot accommodate all known facts, nor because there are facts that apparently disprove it: Hypotheses or theories are abandoned only when there is sufficient acceptance of a plausible and evidently better alternative. In the present instance, there is no obviously salient alternative because the HIV/AIDS dissenters do not agree on a single explanation of what “HIV” and “AIDS” are.

7.3.1There is no monolithic association of “HIV skeptics”, “AIDS Rethinkers”, or as the mainstream would have it, “AIDS denialists”. The only view held in common by all dissenters from HIV/AIDS theory is that “HIV” — no matter what it is or isn’t — doesn’t cause “AIDS”, no matter how that is defined. is typical for people in opposition to mainstream views. Internal disagreements and organizational schisms are common among such “single-issue” groups whose members are not also bound together for other strong overarching and self-interested reasons 810,811.

7.3.2There are specific disagreements over what “HIV” is. Different dissenters hold that: has never been proven to cause AIDS. has never been proven to exist 812. does not exist 812. is a harmless “passenger” virus that opportunistically infects AIDS patients.

7.3.3There is a considerable variety of suggestions about what AIDS is. was a multifactorial syndrome caused by a combination of insults 20. specifically, AIDS-1 resulted from the “fast-lane” lifestyle common among a proportion of gay men during the early years of gay liberation: promiscuous consumption of “recreational” drugs 16, promiscuous sex, frequent infections by gonorrhea, syphilis, etc., indiscriminate consumption of antibiotics even as prophylactics 100, generally unhealthy behavior.

Such behavior damages the intestinal microflora, the immune system’s first line of defense, specifically against the fungal infections that were common in AIDS-1. Such damage brings illness as well as positive “HIV” tests 813,814,815, and explains some of AIDS-2 as well as AIDS-1. was caused specifically by drugs, including ARVs 736,816. So is a proportion of AIDS-2. was and is, and a proportion of AIDS-2 & AIDS-Africa are, a syndrome associated with oxidative stress 80, which can result from a wide range of physical (and even mental) insults (see also sections, 3.2.2,,,,

7.4HIV/AIDS theorists and advocates, and therefore the media and the public, lump together indiscriminately everyone who does not accept the mainstream view in toto, so they do not distinguish between “AIDS Rethinkers” or “HIV Skeptics” who just deny that “HIV” causes “AIDS” by contrast with charlatans and conspiracy theorists 817,818, for example:

7.4.1Peddlers of fake remedies 819.

7.4.2Claims that HIV was man-made 820,821. or accidentally in research on biological warfare 822,823,824. damage certain social groups 825,826,827 — “to depopulate vulnerable target groups, including blacks and other minorities, homosexuals, and perceived ‘decadent’ sexually active individuals” 828, or that condoms sent to Africa were spiked with “HIV” 829.

7.4.3Claims that HIV originated in unrelated cancer 830 or vaccine research or practice 831,832.

7.5The mainstream refuses to engage the evidence or to debate substantively with dissenters.

7.5.1Dissenters are ignored, not answered, boycotted, black-listed, maligned. answered: Duesberg’s seminal article 833 never answered p. 233 in 5; p. 147 in 6; p. 198 in 10; p. 139 ff. in 13; Kary Mullis, request for published proof that HIV causes AIDS pp. 171-4 in 23; Gary Null, asking Robert Gallo to cite publications proving HIV causes AIDS p. 39 in 834 from professional meetings: Peter Duesberg p. 147 in 13 or excluded from professional publications: Peter Duesberg pp. 229-30 in 5; pp. 147-52 in 13; Gordon Stewart pp. 100-31 in 13; pp. 230-1 in 5 permitted to reply to published criticism: Peter Duesberg p. 229 in 5; chapter 3 in 834 no longer funded: Peter Duesberg p. 229 in 5 Various HIV/AIDS skeptics p. 234 in 5 public events canceled: Showing of House of Numbers to be followed by debate 835 at the last moment: Peter Duesberg & Celia Farber, from appearing at Congressional hearing 836 maligned: Various people, as “flat-earthers” pp. 212 & 233-4 in 5 warned against covering dissenting views 837,838,839

7.5.2Where mainstream and dissenters do publicly address the same points, they do not engage with one another. were accused of complicity in deaths in South Africa on the basis of computer-modeled estimates of deaths 523,524,525 that are contrary to the official South Africa Statistics data 74. progressively modified NIH “fact sheet” 840 (most recent revision 14 January 2010) fails to address the specific criticism 25,841 made of its arguments.

7.6The mainstream tries to discredit dissenters via ad hominem polemics 839, not by substantive argument pp. 212 & 233-4 in 5; pp. 49 & 80 in 834.

7.6.1Because the dissenters have never themselves done HIV/AIDS research. is a non sequitur.

Informed individuals are perfectly capable of critiquing the work of others. Peer review of manuscripts and grant proposals is often done by supposedly informed individuals who have not themselves worked on exactly the same topic. Indeed, the advantage of freedom from conflicts of interest makes it desirable that critiques come from other than insiders, be they colleagues or competitors. supporters of the mainstream view and critics of the dissenters — indeed some of the most prominent and vociferous HIV/AIDS proponents — have themselves done no HIV/AIDS research and may not even have any scientific credentials at all 842,843,844: Jeanne Bergman 845 (lawyer) 843,844; Nathan Geffen 846,847 (activist) 848,849; Seth Kalichman 850 (social psychologist) 851; Nicoli Nattrass 523,524,852 (social scientist, economist) 853,854,855. As to the many physicians among public proponents of HIV/AIDS theory, it should be remembered that physicians, doctors, MDs, are not scientists, were not trained to do or to understand research, have no preparation for doing scientific research 856,857. mainstream refers queries to official sources like the NIH “Evidence” 840, but such in- house writings for public consumption are not scientific publications, they are public- relations pieces; they have never been peer-reviewed and are often written by PR personnel, not by scientists. Many official reports are not only not scientific writings, they may be demonstrably incompetent Chapter 8 in 834.

7.6.2Dissenters are labeled denialists 839,850 deliberate analogy with Holocaust deniers is emotionally fraught and is used because the mainstream cannot answer the dissidents’ substantive points 858.’re “flat-earthers” p. 297 in 257.

7.7The media do not cover dissenting views.

7.7.1They fail even to discuss, let alone expose, the improper tactics of those who malign dissenters.


8.1The general context of medical science permits this sort of blunder Chapters 11-13 in 5; 834.

8.1.1Theories once accepted are then not perpetually questioned. that contradict the accepted view are ignored for as long as possible 65,94,859,860,861. are not appreciated. There is no career role in science for inveterate questioners of accepted practices; if possible there is even less room in medical practice for transgressing established practice. review is almost universal as a purported safeguard of quality. In reality, it serves to enshrine whatever the mainstream consensus happens to be 81,526: “Peer review … is simply a way to collect opinions from experts in the field. Peer review tells us about the acceptability, not the credibility, of a new finding” 363.

8.1.2There is no organized coordination of specialized research areas. don’t concern themselves with epidemiology. Clinicians simply accept what the virologists and the drug designers tell them. If data in one specialty are relevant to another specialty, that may not be realized quickly or efficiently. Specialists feel unqualified to critique the specialties of others. much is published that researchers find it difficult to keep up with what everyone is doing even within their own very narrow specialty.

8.2This particular blunder came about via specific identifiable steps Chapters 14 & 15 in 5.

8.2.1Mis-classification of characteristics of AIDS patients: they were primarily drug addicts rather than gay men Chapter 1 & p. 191 ff. in 16.

8.2.2 Mistaking a social phenomenon for a medical one (section 2.1.1).

8.2.3 Accepting inadequate evidence for the presence and activity of a retrovirus (sections 1-3).

8.2.4Once Gallo, with the imprimatur of the Department of Health and Human Services, had been credited with discovery of the probable cause of AIDS, researchers framed their subsequent grant requests and consequent research on the virus hypothesis.

The overwhelming majority of funding of biological research comes from the National Institutes of Health, which is an agency within the Department of Health and Human Services.

8.2.5Alternatives to the retrovirus hypothesis ceased to be discussed by mainstream researchers.

8.2.6Minority views and those of outside observers were peremptorily dismissed.

8.2.7The media did not attend in neutral fashion to dissenting views.

8.3How science and medicine are communicated to the general public entrenches such blunders 314,Chapter 7 in 834 (see also sections 7.1, 7.2, 7.4, 7.7).

8.3.1“a politics dominated by experts and mass persuaders” 174.


9.1If HIV doesn’t cause AIDS, what does cause AIDS?

9.1.1AIDS-1 (the original early-1980s AIDS) resulted from the “fast-lane” lifestyle of drug abuse, extreme promiscuity, and generally unhealthy behavior. The first AIDS victims were in their mid-to-late 30s, consistent with this explanation and inconsistent with a sexually transmitted disease, which affects adolescents and young adults significantly more than others.

9.1.2AIDS-2 (“HIV disease”, “HIV/AIDS”, non-African AIDS) is the mis-interpretation of “HIV” tests whereby anyone who tests “HIV-positive” is presumed to “have HIV/AIDS” — even as authoritative mainstream sources and data demonstrate that innumerable conditions, some but not all of them unhealthy, conduce to testing “HIV-positive”, and even as no “HIV” test has been officially approved for actually identifying active infection.

9.1.3African AIDS is the mis-interpretation of manifest symptoms that are entirely non-specific and moreover are associated with many diseases long endemic in Africa: prolonged fever, cough, diarrhea, bodily wasting (section 2.3.1).

9.2If HIV doesn’t cause AIDS, why do ARVs successfully treat AIDS?

9.2.1They don’t (section 5.1).

ARVs have not increased lifespan — except only when less-toxic combination "cocktails" replaced highly toxic AZT monotherapy. Then there was an immediate decrease in iatrogenic mortality, mortality caused by the medical treatment itself (section 5.1.6).

9.2.2ARVs are very powerful killers of biological systems, and their antibiotic or antifungal or anti- parasitic powers might overcome occult infections; but prolonged use of ARVs is likely to be fatal (sections 5.3, 5.5).

9.3Why do gay men test “HIV-positive” so frequently, if it isn’t an STD?

9.3.1Certain practices common among gay men make testing “HIV-positive” likely, for example, the consequences of intestinal dysbiosis. That condition can also bring on serious illness, including the fungal infections that characterized AIDS-1 (sections,

9.4Questions posed through ignorance of the facts about “HIV” and “AIDS”.

9.4.1“Why are so many mid-life gay men getting HIV?” 492 Because everything about “HIV” and “HIV/AIDS” is most frequent in young middle age, mid-30s to mid-40s (sections, 7.1.1).


1 ^  The doubters;

2 ^  The Perth Group,

3 ^   The Group for the Scientific Reappraisal of the HIV-AIDS Hypothesis;

4 ^  Ian Young, The AIDS Dissidents: An Annotated Bibliography (Scarecrow, 1993).

5 ^ intro | 0.3 | 1.2.3 | 1.2.4 | 1.2.5 | | 3.1 | | 3.2.3 | | 3.3.5 | | 3.3.15 | | 4.7.10 | 4.7.16 | | | | | | | | | | 7.6 | 8.1 | 8.2 | 132 | 166    Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory (McFarland, 2007).

6 ^ intro |    Harvey Bialy, Oncogenes, Aneuploidy and AIDS: A Scientific Life & Times of Peter H. Duesbrrg (Institute of Biotechnology, Autonomous Antional University of Mexico, 2004; ISBN 1-55643-531- 2).

7 ^ intro | 1.2.1    John Crewdson, Science Fictions: A Scientific Mystery, a Massive Cover-Up, and the Dark Legacy of Robert Gallo, Little, Brown (2002).

8 ^  Rebecca Culshaw, Science Sold Out: Does HIV Really Cause AIDS? (North Atlantic Books, 2007); French translation by Pol Dubart, La théorie VIH du SIDA, incohérence scientifique (Résurgence).

9 ^  Etienne de Harven & Jean-Claude Roussez, Ten Lies about AIDS (Trafford, 2008).

10 ^ intro | |    Peter H. Duesberg, Inventing the AIDS Virus (Regnery, 1996); French translation by Pol Dubart, L’invention du virus du sida (Résurgence).

11 ^ intro | 146 | 712    Celia Farber, Serious Adverse Events: An Uncensored History of AIDS (Melville House, 2006).

12 ^ intro | 3.3.18    Christian Fiala, Lieben wir gefährlich? Ein Arzt auf der Suche nach den Fakten und Hintergründen von AIDS (Deuticke, 1997) [Do we love dangerously? A doctor in ssearhc of the facts and background of AIDS].

13 ^ intro | | | |    Neville Hodgkinson, Aids: The Failure of Contemporary Science: How a Virus That Never Was Deceived the World (Fourth Estate, 1996).

14 ^ intro | 4.6.1    F. I. D. Konotey-Ahulu, What is AIDS? (Tetteh-A’Domeno CO., 1989; ISBN 0-9515442-3-3).

15 ^ intro |    Heinrich Kremer, Die stille Revolution der Krebs — und AIDS — Medizin (Wolfratshausen, 2001); English translation by Jamie McIntosh, The Silent Revlolution in Cancer and AIDS Medicine (Xlibris, 2008; ISBN 978-1-4363-5084-6, ISBN 978-1-4363-5083-9).

16 ^ intro | | | 7.1.1 | | 8.2.1    John Lauritsen, The AIDS War: Propaganda, Profiteering and Genocide from the Medical-Industrial Complex (ASKLEPIOS, 1993; ISBN 0-943742-08-0).

17 ^ intro |    John Lauritsen & Ian Young, The AIDS Cult: Essays on the Gay Health Crisis (ASKLEPIOS, 1997; ISBN 0-934742-10-2).

18^  Michael Leitner, Mythos HIV: Eine kritische Analyse der AIDS-Hysterie (Verlag videel OHG [Niebüll], 2000) [Mythical HIV: A Critical Analysis of AIDS Hysteria].

19^  Christine Maggiore, What If Everything You Thought You Knew about AIDS Was Wrong? (American Foundation for AIDS Alternatives, 2007, 4th rev. ed.; ISBN 0-9674153-2 [first ed. 1996]).

20 ^ intro | 3.3.18 | |    Robert S. Root-Bernstein, Rethinking ADS: The Tragic Cost of Premature Consensus (Free Press/Macmillan, 1993).

21^  Joan Shenton, Positively False: Exposing the Myths around HIV and AIDS (I. B. Tauris, 1998).


23 ^ 1.1.1 |    Kary Mullis, Dancing Naked in the Mind Field, Vintage (Random House) 2000, pp. 171-4.

24 ^ 1.1.2 |    Perth Group, “NIH/Antibodies” (contributed to Internet debate preceding Presidential AIDS Advisory Panel meeting, Johannesburg, July 2000);, accessed 23 August 2013.

25 ^ 1.1.2 |    Robert Johnston, Matthew Irwin, & David Crowe, “NIAID/NIH 'Evidence' — Rebuttal”.

26 ^ 1.1.4 |    Lemaître et al., “Protective activity of tetracycline analogs against the cytopathic effect of the human immunodeficiency viruses in CEM cells”, Research in Virology, 141 (1990) 5-16.

27 ^ 1.1.4 |    Lemaître et al., “Role of mycoplasma infection in the cytopathic effect induced by human immunodeficiency virus type 1 in infected cell lines”, Infection and Immunity, 60 (1992) 742-8.

28 ^ 1.1.4 |    S-C Lo, “Mycoplasmas and AIDS”, pp. 525-45 in Maniloff et al. (eds.), Mycoplasmas: molecular biology and pathogenesis, American Society for Microbiology (1992).

29 ^ 1.1.4 |    Blanchard & Montagnier, “AIDS-associated mycoplasmas”, Annual Review of Microbiology, 48 (1994) 687-712.

30 ^ 1.1.4 |    Wang et al., “Mycoplasma penetrans infection in male homosexuals with AIDS: high seroprevalence and association with Kaposi’s Sarcoma”, Clinical Infectious Diseases, 17 (1993) 724-9.

31 ^ 1.1.4 |    Grau et al., “Association of Mycoplasma penetrans with human immunodeficiency virus infection”, Journal of Infectious Diseases,172 (1995) 672-81.

32 ^ 1.1.5 |    P. H. Duesberg, “The HIV gap in national AIDS statistics”, Biotechnology, 11 (1993) 955-6.

33^  A. G. Bird, “Non-HIV AIDS: nature and strategies for its management”, Journal of Antimicrobial Therapy, 37 (suppl. B, 1996) 171-83.

34^  Songok et al., “Low prevalence of human T-lymphotropic virus type I (HTLV-I) in HIV-positive patients in Kenya”, Journal of Acquired Immune Deficiency Syndromes, 7 (1994) 876-7.

35^  Hishida et al., “Clinically diagnosed AIDS cases without evident association with HIV type 1 and 2 infections in Ghana”, Lancet, 340 (1992) 971-2.

36^  In August 2013, PubMed listed >260 articles about idiopathic CD4 T-cell lymphopenia.

37^  “Unexplained CD4+ T-lymphocyte depletion in persons without evident HIV infection — United States”, MMWR, 41(#30, 1992) 541-5; JAMA, 268 (1992) 1254-5.

38^  Smith et al., “Unexplained opportunistic infections and CD4+ T-lymphocytopenia without HIV infection. An investigation of cases in the United States. The Centers for Disease Control Idiopathic CD4+ T-lymphocytopenia Task Force”, New England Journal of Medicine, 328 (1993) 373-9.

39^  Spira et al., “Idiopathic CD4+ T-lymphocytopenia — an analysis of five patients with unexplained opportunistic infections”, New England Journal of Medicine, 328 (1993) 386-92.

40^  Mukherjee et al., “Idiopathic CD4+ T-cell lymphocytopenia”, Indian Journal of Pediatrics, 76 (2009) 430-20.

41^  Ho et al., “Idiopathic CD4+ T-lymphocytopenia--immunodeficiency without evidence of HIV infection”, New England Journal of Medicine, 328 (1993) 380-5.

42^  Famularo et al., “The syndrome of idiopathic CD4+ lymphocytopenia”, Annali Italiani di Medicina Interna, 9 (1994) 22-6.

43^  A. Fauci, “CD4+ T-lymphocytopenia without HIV infection — no lights, no camera, just facts”, New England Journal of Medicine, 328 (1993) 429-31.

44^  Browne et al., “Adult-Onset Immunodeficiency in Thailand and Taiwan”, New England Journal of Medicine, 367 (2012) 725-34.

45 ^ 1.1.6 | 1.3    Henry H. Bauer, “‘HIV/AIDS’ deaths: often not from ‘HIV’ nor from ‘AIDS’!”,

46^  Henry H. Bauer, “Official Italian data: no causal connection between HIV and AIDS”,

47^  Henry H. Bauer, “Italy: Demographics of HIV and AIDS”,

48^  Henry H. Bauer, “No HIV epidemic in Italy”,

49 ^ 1.2.1 | 3.1.2    Gallo et al., “Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS”, Science, 224 (1984) 500-3.

50 ^ 1.2.1 |    Papadopulos-Eleopulos et al., “Has Gallo proven the role of HIV in AIDS?”, Emergency Medicine [Australia], 5 (1993) 113-23.

51^  Serge Lang, “The Gallo Case”, pp. 361-600 in Challenges (Springer, 1998).

52^  Bernard Dixon, “Citation analysis and HIV”, Bio/technology, 12 (1994) 1050.

53^  Wong-Staal & Gallo, “Human T-lymphotropic retroviruses”, Nature, 317 (1985) 395-403.

54^  Beral et al., “Kaposi's sarcoma among persons with AIDS: a sexually transmitted infection?”, Lancet, 335 (1990) 123-8.

55^  O'Brien et al., “Evidence for concurrent epidemics of human herpesvirus 8 and human immunodeficiency virus type 1 in US homosexual men: rates, risk factors, and relationship to Kaposi's sarcoma”, Journal of Infectious Diseases, 180 (1999) 1010-7.

56^  Renwick et al., “Seroconversion for human herpesvirus 8 during HIV infection is highly predictive of Kaposi's sarcoma”, AIDS, 12 (1998) 2481-8.

57^  Engels et al., “Detection and quantification of Kaposi's sarcoma-associated herpesvirus to predict AIDS-associated Kaposi's sarcoma”, AIDS, 17 (2003) 1847-51.

58^  Richetta et al., “PEL, Kaposi's sarcoma HHV8+ and idiopathic T-lymphocitopenia CD4+”, Clinica Terapeutica, 158 (2007) 151-5.

59^  Newell et al., “Toxicity, immunosuppressive effects and carcinogenic potential of volatile nitrites: Possible relationship to Kaposi's sarcoma”, Pharmacotherapy, 4 (1984) 284-91.

60^  John Lauritsen & Hank Wilson, DEATH RUSH: Poppers and AIDS, New York: Pagan Press, 1986; ISBN 0-943742-05-6.

61^  Papadopulos-Eleopulos et al., “Kaposi's Sarcoma and HIV”, Medical Hypotheses, 39 (1992) 22-9.

62^  Newell et al., “Volatile nitrites. Use and adverse effects related to the current epidemic of the acquired immune deficiency syndrome”, American Journal of Medicine, 78 (1985) 811-6.

63^  Newell et al., “Risk factor analysis among men referred for possible Acquired Immune Deficiency Syndrome”, Preventive Medicine, 14 (1985) 81-91.

64 ^ |    John Lauritsen, “NIH reconsiders nitrites’ link to AIDS”, Bio/technology, 12 (1994) 762-3.

65^  Thomas S. Kuhn, The Structure of Scientific Revolutions (University of Chicago Press, 1970 [2nd ed., enlarged; 1st ed. 1962]).

66^  Henry H. Bauer, “‘HIV disease’ is not an illness”,

67^  Henry H. Bauer, “How ‘AIDS Deaths’ and ‘HIV Infections’ vary with age — and why”,

68 ^ 1.3.1 | 5.1 | 5.1.5 | 5.1.6    Henry H. Bauer, “HAART saves lives — but doesn’t prolong them!?”,

69^  Henry H. Bauer, “Living with HIV; Dying from what?”,

70^  Henry H. Bauer, “HIV, AIDS, and age: HIV/AIDS theory is wrong”,

71^  Henry H. Bauer, “Age shall not wither them — because HIV really doesn’t kill”,

72^  Matteo Payer Galletti and Henry H. Bauer, “Safety issues in didactic anatomical dissection in regions of high HIV prevalence”, Italian Journal of Anatomy and Embryology, 114 (#4, 2009) 179-192;

73^  Henry H. Bauer, “What numbers mean: 50% of ‘HIV-positives’ are long-term non-progressors”,

74 ^ 1.3.2 | 4.5.5 |    Duesberg et al., “AIDS since 1984: No evidence for a new, viral epidemic — not even in Africa”, Italian Journal of Anatomy and Embryology,116 (2011) 73-92.

75^  “The Pathogenesis of AIDS” (updated 8 April 2009),, accessed 9 August 2013.

76^  Peter H. Duesberg, “Retroviruses as Carcinogens and Pathogens: Expectations and Reality”, Cancer Research, 47 (1987) 1199-1220.

77^  “Pneumocystis Pneumonia --- Los Angeles”, MMWR, 30 (21, 5 June 1981) 1-3.First descriptions of AIDS cases

78^  “Current Trends Update on Acquired Immune Deficiency Syndrome (AIDS) — United States”, MMWR, 31 (37, 24 September 1982) 507-8, 513-4.

79^  Mongardon et al., “Pneumonia involving Mycobacterium tuberculosis and Pneumocystis jiroveci in HIV-seronegative patients”, European Journal of Internal Medicine,19 (2008) e70-2.

80 ^ 1.2.3 | | | |    Eleni Papadopulos-Eleopulos, “Reappraisal of Aids: Is the oxidation induced by the risk factors the primary cause?”, Medical Hypotheses 25 (1988) 151-62.

81^  Steinhauser et al., “Peer review versus editorial review and their role in innovative science”, Theoretical Medicine and Bioethics, 33 (2012) 359-76.

82^  Kony et al., “Tuberculosis-associated severe CD4+ T-Lymphocytopenia in HIV-seronegative patients from Dakar”, Journal of Infection, 41 (2000) 167-71.

83^  Onorati et al., “CD4 T-lymphocytopenia and Pneumocystis carinii pneumonia in a patient with miliary tuberculosis”, European Journal of Internal Medicine, 12 (2001) 134-6.

84^  Nelson Vergel, “There when AIDS began: An interview with Michael Gottlieb, M.D., 2 June 2011;

85^  Mientjes et al., “Frequent injecting impairs lymphocyte reactivity in HIV-positive and HIV-negative drug users”, AIDS, 5 (1991) 35-41.

86^  Donahoe et al., “Mechanistic implications of the findings that opiates and other drugs of abuse moderate T-cell surface receptors and antigenic markers”, Annals of the New York Academy of Sciences, 496 (1987) 711-21.

87^  Pacifici et al., “Effects of repeated doses of MDMA (‘ecstasy’) on cell-mediated immune response in humans”, Life Sciences, 69 (2001) 2931-41.

88 ^ | 3.3.9    Duesberg & Rasnick, “The AIDS dilemma: drug diseases blamed on a passenger virus”, Genetica, 104 (1998) 85-132.

89^  Lazzarin et al., “Impairment of polymorphonuclear leucocyte function in patients with acquired immunodeficiency syndrome and with lymphadenopathy syndrome”, Clinical and Experimental Immunology, 65 (1986) 105-11.

90^  Des Jarlais et al., “Development of AIDS, HIV seroconversion, and potential co-factors for T4 cell loss in a cohort of intravenous drug users”, AIDS, 1(1987) 105-11.

91^  Newell et al., “Toxicity, immunosuppressive effects and carcinogenic potential of volatile nitrites: possible relationship to Kaposi's sarcoma”, Pharmacotherapy, 4 (1984) 284-91.

92^  Hersh et al., “Effect of the recreational agent isobutyl nitrite on human peripheral blood leukocytes and on in vitro interferon production”, Cancer Research, 43 (1983) 1365-71.

93^  Ruiz et al., “Human T lymphocyte subpopulation and NK cell alterations in persons exposed to cocaine”, Clinical Immunology and Immunopathology, 70 (1994) 245-50.

94^  Ernest B. Hook, (ed)., Prematurity in Scientific Discovery: On Resistance and Neglect (University of California Press, 2002).

95 ^ | 7.1.1    Michelle Cochrane, When AIDS Began: San Francisco and the Making of an Epidemic (Routledge, 2004).

96^  Moss et al., “Risk factors for AIDS and HIV seropositivity in homosexual men”, American Journal of Epidemiology, 125 (1987) 1035-47.

97^  Jaffe et al., “National case-control study of Kaposi's sarcoma and Pneumocystis carinii pneumonia in homosexual men: Part 1. Epidemiologic results”, Annals of Internal Medicine, 99 (1983) 145-51.

98^  Rogers et al., “National case-control study of Kaposi's sarcoma and Pneumocystis carinii pneumonia in homosexual men: Part 2. Laboratory results”, Annals of Internal Medicine, 99 (1983) 151-8.

99 ^ |    Larry Kramer, Faggots (Random House, 1978).

100 ^ | |    When Ocean Meets Sky (film by Crayton Robey, 2003);

101 ^ |    Michael Callen, Surviving AIDS (HarperCollins, 1990).

102^  Richard Berkowitz, Stayin' alive: the invention of safe sex (Westview, 2003).

103 ^ | 2.1.2    Gottlieb et al., “Epidemiologic Notes and Reports: Pneumocystis Pneumonia — Los Angeles”, MMWR, 30 (#21, 5 June 1981) 1-3.

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292^  Neale et al., “False-positive anti-HTLV-III serology”, New Zealand Medical Journal, 98 (1985) 914.

293^  Burkhardt et al., “Comparison of two commercially available anti-HIV ELISA's: Abbott HTLV-III ELA and DuPont HTLV-III ELISA”, Journal of Medical Virology, 23 (1987) 217-24.

294^  A. Voevodin, “HIV screening in Russia”, Lancet, 339 (1992) 1548.

295^  Magee et al., “False-positive results in antenatal HIV screening”, Canadian Medical Association Journal, 160 (1999) 1285.

296^  Shima-Sano et al., “A HIV screening algorithm to address the high rate of false-positive results in pregnant women in Japan”, PLoS ONE, 5 (2010) e9382.

297^  Zacharias et al., “High false-positive rate of HIV rapid serum screening in a predominantly Hispanic prenatal population”, Journal of Perinatology, 24 (2004) 743-7.

298^  “HIV demographics are predictable; HIV is not a contagious infection”,; “Why pregnant women tend to test ‘HIV-positive’”,

299^  Taha et al., “Trends of HIV-1 and sexually transmitted diseases among pregnant and postpartum women in urban Malawi”, AIDS, 12 (1998) 197-203.

300^  Rwakyendela et al., “The rate of HIV seroconversion occurring during pregnancy in women who tested negative at their first antenatal booking at Chris Hani Baragwanath Hospital, Soweto”, 8th Reproductive Health Priorities Conference, Wild Coast (South Africa), October 2002; cited in James A. McIntyre, “Sex, pregnancy, hormones, and HIV”, Lancet, 366 (2005) 1141-2.

301^  Jewkes et al., “Relationship dynamics and teenage pregnancy in South Africa”, Social Science and Medicine, 52 (2001) 733-44.

302^  Stuart W. Dwyer, “President Mbeki might have a case on rethinking AIDS”, British Medical Journal, 324 (2002) 237;

303^  Craig Timberg, “How AIDS in Africa was overstated”, Washington Post, 6 April 2006;

304 ^ |    Chris Baryomunsi, “Uganda: rising HIV infection — Where did we lose it?”, New Vision (Kampala), 12 December 2006;

305^  Mugo et al., “Increased risk of HIV-1 transmission in pregnancy: a prospective study among African HIV-1-serodiscordant couples”, AIDS, 25 (2011) 1887-95.

306^  Horwitz et al., “Novel human endogenous sequences related to human immunodeficiency virus type 1”, Journal of Virology, 66 (1992) 2170-9.

307^  McClure et al., “Automated characterization of potentially active retroid agents in the human genome”, Genomics, 85 (2005) 512-23.

308^  Yang et al., “An ancient family of human endogenous retroviruses encodes a functional homolog of the HIV-1 Rev protein”, Proceedings of the National Academy of Sciences USA, 96(1999) 13404-8.

309^  Etienne de Harven, “Human Endogenous Retroviruses and AIDS research: Confusion, consensus, or science?” Journal of American Physicians and Surgeons, 15 (#3, 2010) 69-74,; and press release: “Human Endogenous Retroviruses can resolve HIV/AIDS puzzles”,

310^  Nakagawa & Harrison, “The potential roles of endogenous retroviruses in autoimmunity”, Immunological Reviews, 152 (1996) 193-236.

311^  Löwer et al., “The viruses in all of us: characteristics and biological significance of human endogenous retrovirus sequences”, Proceedings of the National Academy of Sciences USA, 93 (1996) 5177-84.

312 ^ 4.7.15 |    David Rasnick, "AIDS drugs cause AIDS and death", ch. 11, pp. 237-50, in Marco Mamone Capria (ed.) Science and the Citizen: Contemporary Issues and Controversies, 2013; ISBN 978-1-291-44683-8. Free PDF download of the full text is available at

313^  “Serological diagnosis of human immunodeficiency virus infection by Western blot testing. The Consortium for Retrovirus Serology Standardization”, JAMA, 260 (1988) 674-9.

314^  Michael Tracey, "Mere smoke of opinion: Aids and the making of the public mind," Inaugural lecture, Chair of International Communication, University of Salford (England) 1995;

315^  Parmentier et al., “Epitopes of human immunodeficiency virus regulatory proteins tat, nef, and rev are expressed in normal human tissue”, American Journal of Pathology, 141 (1992) 1209-16.

316^  Lyden et al., “Expression of endogenous HIV-1 crossreactive antigens within normal human extravillous trophoblast cells”, Journal of Reproductive Immunology, 28 (1995) 233-45.

317^  Cook et al., “Effects of alcohol and crack/cocaine use on virological and immunological disease progression in a cohort of U.S. women with HIV/AIDS”, XVI International ADS Conference, Toronto, 13-18 August 2006

318^  Cook et al., “Crack cocaine, disease progression, and mortality in a multicenter cohort of HIV-1 positive women”, AIDS, 22 (2008) 1355-63.

319^  “HIV Prevention Campaign Targets Meth Use in Gay Community”, 1 July 2007;, accessed 10 July 2007.

320 ^ |    Spencer Cox & Bruce Kellerhouse, “The authors respond”, 21 March 2007;, accessed 25 March 2007.

321^  Cooper et al., “Vaccine-induced HIV seropositivity/reactivity in noninfected HIV vaccine recipients”, JAMA, 304 (2010) 275-83.

322^  MacKenzie et al., “Multiple false-positive serologic tests for HIV, HTLV-1, and hepatitis C following influenza vaccination, 1991”, JAMA, 268 (1992) 1015-7.

323^  Lee et al., “HIV false positivity after hepatitis B vaccination”, Lancet, 339 (1992) 1060.

324^  S. Isaacman, “Positive HIV antibody test results after treatment with hepatitis B immune globulin”, JAMA, 262 (1989) 209.

325^  Araujo et al., “Rubella vaccination and transitory false-positive test results for HIV Type 1 in blood donors”, Transfusion, 49 (2009) 2516-17.

326^  Gonnelli et al., “Transiently positive HIV antibody test after treatment with tetanus immune globulin”, Lancet, 337 (1991) 731.

327^  Deuchert & Brody , “The role of health care in the spread of HIV/AIDS in Africa: evidence from Kenya”, International Journal of STD & AIDS, 17 (2006) 749-52.

328^  Saag et al., “HIV viral markers in clinical practice”, Nature Medicine, 2 (1996) 625-9.

329 ^ |    Victoria Stagg Elliott, “Use of HIV testing in ED hits snags”, American Medical News, 4 June 2007;

330 ^ 3.3.1 | 3.3.2    Padian et al., “Heterosexual transmission of human immunodeficiency virus (HIV) in Northern California: results from a ten-year study," American Journal of Epidemiology, 146 (1997) 350–7.

331^  Barreiro et al., “Natural pregnancies in HIV-serodiscordant couples receiving successful antiretroviral therapy”, Journal of Acquired Immune Deficiency Syndromes, 43 (2006) 324-6.

332^  Hayley Ringle, “Man’s adoptions take the negative out of HIV”, East Valley Tribune (AZ), 1 May 2006; 0fa89198bf39.html?mode=story

333 ^ |    Papadopulos-Eleopulos et al., Mother to Child Transmission of HIV and Its Prevention with AZT and Nevirapine: A Critical Analysis of the Evidence, The Perth Group, October 2001;

334 ^ | 4.7.9    “More HIV, less infection: The breastfeeding conundrum”,; “HIV and breastfeeding again”,

335^  Coovadia et al., “Mother-to-child transmission of HIV-1 infection during exclusive breastfeeding in the first 6 months of life: an intervention cohort study”, Lancet, 369 (2007) 1107-16.

336^  Horvath et al., “Interventions for preventing late postnatal mother-to-child transmission of HIV”, Cochrane Database Syst Rev, 21 Jan 2009, (1):CD006734.

337^  Theo Smart, HATIP (HIV & AIDS Treatment in Practice),#74, 12 September 2006;

338^  Rebecca Goldin, “HIV and Breastfeeding”, Statistical Assessment Service, George Mason University (Washington, DC), 23 April 2007;

339^  Gisselquist et al., “HIV infections in sub–Saharan Africa not explained by sexual or vertical transmission”, International Journal of Sexually Transmitted Diseases and AIDS, 13 (2002) 657-66.

340^  “Mystery shrouds detection of HIV in 18-month-old”, The Hindu, 20 March 2013;

341^  Henry H. Bauer, “HIV demographics are predictable; HIV is not a contagious infection”,

342^  Henry H. Bauer, “‘HIV’ epidemiology disproves HIV/AIDS theory”,

343^  Henry H. Bauer, “HIV, AIDS, and age: HIV/AIDS theory is wrong”,

344^  Henry H. Bauer, “Deaths from ‘HIV disease’: Why has the median age drifted upwards?”,

345^  Henry H. Bauer, “No HIV ‘latent period’: dotting i’s and crossing t’s”,

346^  Henry H. Bauer, “Age shall not wither them — because HIV really doesn’t kill”,

347^  Henry H. Bauer, “How ‘AIDS deaths’ and ‘HIV infections’ vary with age — and WHY”,

348 ^ 3.3.6 | 6.2.3    “OMSJ Defense Wins 52nd Case”,

349^  Victoria A. Harden, AIDS at 30 (Potomac Books, 2012) p. 232.

350^  “How antibodies fight HIV: New evidence”, 7 September 2007;

351^  Mascola, “Allied responses”, Nature, 449 (2007) 29-30.

352^  Hessell et al., “Fc receptor but not complement binding is important in antibody protection against HIV”, Nature, 449 (2007) 101-4.

353^  “Ending AIDS: The search for a vaccine”, PBS television, 1 December 2005.

354^  Margaret Heckler, cited at p. 25 in The AIDS Bureaucracy by Sandra Panem (Harvard University Press, 1988).

355^  Victoria A. Harden, AIDS at 30: A History (Potomac Books, 2012) p. 64.

356^  Hal Hellman, Great Feuds in Medicine (Wiley, 2002) p. 176.

357 ^ 3.3.7 | 4.1.7    Henry H. Bauer, "Holy Grails, Unicorns, and HIV Vaccines".

358^  Bruneau et al., “High rates of HIV infection among injection drug users participating in needle exchange programs in Montreal: results of a cohort study, American Journal of Epidemiology, 146 (1997) 994-1002.

359^  Krueger et al., “Poverty and HIV seropositivity: the poor are more likely to be infected”, AIDS, 4 (1990) 811–4.

360 ^ | 3.3.19    Moss, et al., “HIV seroconversion in intravenous drug users in San Francisco, 1985-90”, AIDS, 8 (1994) 223–31.

361^  Kral et al., “HIV prevalence and risk behaviors among men who have sex with men and inject drugs in San Francisco”, Journal of Urban Health: Bulletin of the New York Academy of Medicine, 82 (#1, Suppl. 1, 2005) i43-50.

362^  Page-Shafer et al., “Sexual risk behavior and risk factors for HIV-1 seroconversion in homosexual men participating in the Tricontinental Seroconverter Study, 1982-1994”, American Journal of Epidemiology, 146 (1997) 531-42.

363^  Richard Horton, Health Wars: On the Global Front Lines of Modern Medicine (New York Review Books, 2003) p. 306

364^  Ran Reznick, “Keeping the disease under wraps”, 5 August 2007;

365^  Dr. Rashmi Shukla, regional director of public health for the West Midlands, “Patient tests offered after hospital worker diagnosed with HIV”, 7 November; 2006;

366^  Henry H. Bauer, “Condoms and HIV: What everyone knows is once again wrong”,

367^  Henry H. Bauer, “Spontaneous generation of ‘HIV’”,

368^  Henry H. Bauer, “Circumcision and condom idiocies”,

369^  Henry H. Bauer, “Porn industry proves that ‘HIV’ is not sexually transmitted”,

370^  Henry H. Bauer, “Porn Industry even freer of ‘HIV’ than earlier admitted”,

371^  Henry H. Bauer, “More porn”,

372^  Goldstein et al., “High chlamydia and gonorrhea incidence and reinfection among performers in the adult film industry”, Sexually Transmitted Diseases, 38 (2011) 644-8.

373 ^ 3.3.12 | 4.1.2 | 4.5.1 |    James Chin, The AIDS Pandemic: The Collision of Epidemiology with Political Corectness (Radcliffe, 2007).

374^  Henry H. Bauer, “Why UNAIDS should be disbanded”,

375 ^ 3.3.14 |    Henry H. Bauer, “Race and sexual behavior: Stereotype vs. fact”,

376^  Maulsby et al., “HIV Among black men who have sex with men (MSM) in the United States: A review of the literature”, AIDS and Behavior, 26 April 2013 [Epub ahead of print] DOI 0.1007/s10461-013-0476-2.

377^  Wawer et al., “Control of sexually transmitted diseases for AIDS prevention in Uganda: a randomised community trial. Rakai Project Study Group”, Lancet, 353 (1999) 525-35.

378^  Rothenberg et al., “Concurrency and sexual transmission”, AIDS, 16 (2002) 678-9.

379^  Henry H. Bauer, “To avoid HIV infection, don’t get married”,;

380^  Henry H. Bauer, “Abstinence-based HIV programs in Africa may put married women at risk”,

381^  Christian Fiala, “Epidemiological evidence against heterosexual transmission of HIV and against prevention-campaigns”, 25 June 2000;

382^  Rosenberg & Weiner, “Prostitutes and AIDS: a health department priority?”, American Journal of Public Health, 78 (1988) 418-23.

383^  “HIV among African Americans”, Fact Sheet, Centers for Disease Control & Prevention;

384^  “HIV Incidence”, Fact Sheet, Centers for Disease Control & Prevention;

385^  “HIV Among Black/African American Gay, Bisexual, and Other Men Who Have Sex With Men”, Fact Sheet, Centers for Disease Control & Prevention;

386^  Chaisson et al., “Racial heterogeneity of HIV antigenemia in people with HIV infection”, AIDS, 5 (1991) 177-80.

387^  Dyer et al., “High levels of human immunodeficiency virus type 1 in blood and semen of seropositive men in sub-Saharan Africa”, Journal of Infectious Diseases, 177 (1998) 1742-6.

388^  Craddock et al., “Predominance of one T-cell antigen receptor BV haplotype in African populations”, Immunogenetics, 51 (2000) 231-7.

389^  Joint United Nations Programme on HIV/AIDS (UNAIDS), UNAIDS report on the global AIDS epidemic 2012, ISBN 978-92-9173-996-7.

390^  Sheila Crisostomo, The Philippine Star, 9 July 2007: “2,916 HIV cases since 1984” instead of 10,000 predicted 5 years earlier.

391^  Beth Barrett, “‘An HIV epidemic could happen’ — health officials say safety standards are ignored — some studios are flouting condom rules”, Daily News (Los Angeles, CA), 4 June 2007;

392^  Helen Epstein, The Invisible Cure: Why We Are Losing the Fight Against AIDS in Africa, (Farrar, Straus and Giroux, 2007).

393^   Fresh population concerns in Africa”, People & Planet, 29 Oct 2007.

394^  Trautmann et al., “Upregulation of PD-1 expression on HIV-specific CD8+ T cells leads to reversible immune dysfunction”, Nature Medicine, 12 (2006) 1198-202 — “Montreal researchers make a major strategic breakthrough in controling the AIDS virus”,

395^  Marie McCullough, “Gene therapy shows promise against HIV”, 7 November 2006;

396^  Randy Dotinga, “Gene therapy shows promise against HIV”, 19 February 2010;

397^  Anderson et al., “Safety and efficacy of a lentiviral vector containing three anti-HIV genes — CCR5 ribozyme, Tat-rev siRNA, and TAR decoy—in SCID-hu mouse–derived T cells”, Molecular Therapy, 15 (2007) 1182-8.

398^  Rossi et al., “Genetic therapies against HIV”, Nature Biotechnology, 25 (2007) 1444-54.

399^  “Scientists close in on anti-HIV protein”, 29 December 2006;, accessed 3 August 2013 (referring to Woo et al., “Structural basis for protein recognition by B30.2/SPRY domains”, Molecular Cell, 24 (2006) 967-76.

400^  “Viral Genetics identifies crucial peptides for potential HIV/AIDS drug”, 1 January 2007;

401^  Dimitrova et al., “Inhibition of HIV type 1 replication in CD4+ and CD14+ cells purified from HIV type 1-infected individuals by the 2-5A agonist immunomodulator, 2-5A(N6B)”, AIDS Research & Human Retroviruses, 23 (2007) 123-34.

402^  De Witte et al., “Langerin is a natural barrier to HIV-1 transmission by Langerhans cells”, Nature Medicine, 13 (2007) 367-71.

403^  Bell et al., “Synthesis and structure-activity relationship studies of CD4 down-modulating cyclotriazadisulfonamide (CADA) analogues”, Journal of Medicinal Chemistry, 49 (2006) 1291-312.

404^  Demillo et al., “Unsymmetrical cyclotriazadisulfonamide (CADA) compounds as human CD4 receptor down-modulating agents”, Journal of Medicinal Chemistry, 54 (2011) 5712-21.

405^  “CybeRelease: (OTC: AMZB) Gets Patent for Treating HIV Infections”, WEBWIRE, 16 February 2007;

406^  “Novel antiviral HIV drug SpirH™ offers new hope for AIDS patients worldwide”, 9 October 2007, Canopus Biopharma;

407^  Anna Canale-Parola, “Potent HIV killer found in alligator blood”, 7 April 2008;

408^  Welch et al., “Potent D-peptide inhibitors of HIV-1 entry”, Proceedings of the National Academy of Sciences USA, 104 (2007) 16828-33.

409^  Welch et al., “Design of a potent D-peptide HIV-1 entry inhibitor with a strong barrier to resistance”, Journal of Virology, 84 (2010) 11235-44.

410^  Bakkour et al., (2007) “Small-molecule inhibition of HIV pre-mRNA splicing as a novel antiretroviral therapy to overcome drug resistance”, PLoS Pathogen, 3 (2007) e159;

411^  Cynthia Graber, “Hepatitis may be ally against HIV: A part of one of the proteins of the Hepatitis C virus shows anti-HIV activity in cell cultures” (podcast), Scientific American 60-Second Science, 1 April 2008.

412^  Soares et al., “Targeting inside-out phosphatidylserine as a therapeutic strategy for viral diseases”, Nature Medicine, 14 (2008) 1357-62.

413^  Alan Engleman, “A reversal of fortune in HIV-1 integration”, Science, 316 (2007) 1855-7.

414^  Sarkar et al., “HIV-1 Proviral DNA Excision Using an Evolved Recombinase”, Science, 316 (2007) 1912-5.

415^  Donzella et al., “AMD3100, a small molecule inhibitor of HIV-1 entry via the CXCR4 co-receptor”, Nature Medicine, 4 (1998) 72-7.

416^  Hendrix et al., “Safety, pharmacokinetics, and antiviral activity of AMD3100, a selective CXCR4 receptor inhibitor, in HIV-1 infection”, Journal of Acquired Immune Deficiency Syndromes, 37 (2004) 1253-62.

417^  Tcherepanova et al., “Multiplex RT-PCR amplification of HIV genes to create a completely autologous DC-based immunotherapy for the treatment of HIV infection”, PLoS ONE, 3 (2008) e1489.

418^  Kashman et al., “The calanolides, a novel HIV-inhibitory class of coumarin derivatives from the tropical rainforest tree, Calophyllum lanigerum”, Journal of Medicinal Chemistry, 35 (1992) 2735-43.

419^  “‘Body armour’ to fight HIV”, Scotsman, 13 May 2006;

420^  Robert Gallo, Virus Hunting: AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery (Basic Books, 1991) p. 296.

421 ^ 4.2.2 | 4.2.4    Cooper & Pantaleo, “Thirty years of HIV: what have we learned?”, Current Opinion in HIV & AIDS, 8 (2013) 304-5.

422^  Tamara McLean, “Global warming set to fan the HIV fire”, The Sydney Morning Herald, 29 April 2008.

423^  Altfeld & Markowitz, “Acute HIV-1 infection: past lessons, current thinking, future goals”, Current Opinion in HIV & AIDS, 3 (2008) 1-3.

424^  F. D. Goebel, “Clinical manifestations of acquired immunologic deficiency syndrome (AIDS)”, Acta Med Austriaca, 14 (1987) 1-4.

425^  Eberhartinger & Simader, “Acute AIDS-retrovirus infection. Clinical picture in a patient with HTLV- III seroconversion”, Wiener Klinische Wochenschrift, 99 (1987) 18-20.

426^  Piette et al., “Acute symptomatology in primary HIV virus infection”, Presse Med, 16 (1987) 346-8.

427^  Cooper et al., “Acute AIDS retrovirus infection: Definition of a clinical illness associated with seroconversion”, Lancet, 1 (8428, 9 March 1985) 537-40.

428^  Lindskov et al., “Acute HTLV-III infection with roseola-like rash”, Lancet, 1 (8478, 22 February 1986) 447.

429^  Gelgor & Kaldor, “Epidemiology of primary HIV-1 infection”, Current Opinion in HIV and AIDS, 3 (2008) 4-9.

430^  Daar et al., “Transient high levels of viremia in patients with primary human immunodeficiency virus type 1 infection”, New England Journal of Medicine, 324 (1991) 961-4.

431^  Kessler et al., “Diagnosis of human immunodeficiency virus infection in seronegative homosexuals presenting with an acute viral syndrome”, JAMA, 258 (1987) 1196-9.

432^  Finkbeiner, “AIDS: just the facts from specialists at Johns Hopkins”, Johns Hopkins Magazine, December 1985, pp. 23-8.

433^  Richardson et al., “Acute HIV Infection among Kenyan Infants”, Clinical Infectious Diseases, 46 (2008) 289-95.

434^  “The Pathogenesis of AIDS”,

435^  Henry et al., “Explaining, predicting, and treating HIV-associated CD4 cell loss: After 25 years still a puzzle”, JAMA, 296 (2006) 1523-5.

436^  M. Stevenson, “HIV-1 pathogenesis”, Nature Medicine, 9 (2003) 853-60.

437 ^ 4.2.6 |    Forsman & Weiss, “Why is HIV a pathogen?”, Trends in Microbiology, 16 (2008) 555-60.

438^  Keele et al., “Chimpanzee reservoirs of pandemic and nonpandemic HIV-1”, Science, 313 (2006) 523-6.

439^  H. A. Stephens, “HIV-1 diversity versus HLA class I polymorphism”, Trends in Immunology, 26 (2005) 41-7.

440^  Shawn J. Green, “Gut mucosa in HIV infection: ‘Immune milk’ solution”, PLoS Medicine, 4 (February 2007) e84-5.

441^  Vujkovic-Cvijin et al., “Dysbiosis of the Gut Microbiota Is Associated with HIV Disease Progression and Tryptophan Catabolism”, Science Translational Medicine, 5 (2013) 193ra91.

442^  Irvine et al., “Probiotic yogurt consumption is associated with an increase of CD4 count among people living with HIV/AIDS”, Journal of Clinical Gastroenteroogyl, 44 (2010) e201-5.

443^  Bruce Pannier, “Kyrgyzstan: Officials investigate accidental HIV/AIDS infections”, 1 August 2007, RFE/RL (Radio Free Europe/Radio Liberty);

444^  Henry H. Bauer, “Immaculate infection by HIV”,

445^  Hitti et al., “Protective effect of vaginal Lactobacillus on genital HIV-1 RNA concentrations: Longitudinal data from a US cohort study”, 15th Conference on Retroviruses and Opportunistic Infections, Boston, 2008, abstract 27LB.

446^  Gus Cairns & Virginia Differding, "CROI: Lactobacillus supplementation could help reduce vaginal HIV," nam-aidsmap, 5 February 2008;

447^  “Hundreds may have HIV without knowing”, Scotsman, 5 June 2007;

448^  Crystal Phend, “AACAP: HIV-infection in children leads to more psychiatric symptoms”, 31 October 2006;

449^  Owe-Larsson et al., “HIV infection and psychiatric illness”, African Journal of Psychiatry (Johannesbg), 12 (2009) 115-28.

450^  Modi et al., “Human immunodeficiency virus associated intracranial aneurysms: report of three adult patients with an overview of the literature”, Journal of Neurology and Neurosurgical Psychiatry, 79 (2008) 44-6.

451^  Goldstein et al., “HIV-associated intracranial aneurysmal vasculopathy in adults”, Journal of Rheumatology, 37 (2010) 226-33.

452^  Bozzette et al., “Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection”, New England Journal of Medicine, 348 (2003) 702-10.

453^  “HIV and arthritis: What's the connection?”,

454 ^ | |    Rob Dawson, “IAS: Aging with HIV — are cancer, heart disease, dementia the new challenges?”, 30 July 2007;

455^  Nakimuli-Mpungu et al., “Primary mania versus HIV-related secondary mania in Uganda”, American Journal of Psychiatry, 163 (2006) 1349-54, quiz 1480; PubMed: 16877646.

456^  Nakimuli-Mpungu et al., “Early-onset versus late-onset HIV-related secondary mania in Uganda”, Psychosomatics, 49 (2008) 530-4.

457^  Nakimuli-Mpungu et al., “Clinical presentation of bipolar mania in HIV-positive patients in Uganda”, Psychosomatics, 50 (2009) 325-30.

458^  Triant et al., “Increased acute myocardial infarction rates and cardiovascular risk factors among patients with Human Immunodeficiency Virus Disease”, Journal of Clinical Endocrinology and Metabolism, 92 (2007) 2506-12.

459^  Klein et al., “Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection?”, Journal of Acquired Immune Deficiency Syndromes, 30 (2002) 471-7.

460 ^ |    “Types of Peripheral Neuropathy — Inflammatory — HIV / AIDS”, Center for Periphreal Neuropathy, University of Chicago;

461 ^ |    “HIV neuropathy”, Peripheral Nerve Center, Johns Hopkins University;

462 ^ |    “Study of NGX-4010 for the treatment of painful HIV-associated neuropathy”, Clinical Trial NCT00321672;

463^  Ross & Klotman, “Recent progress in HIV-associated nephropathy”, Journal of the American Society of Nephrology, 13 (2002) 2997–3004.

464^  Aditi Tandon, “PGI Study: Greater exposure to HIV virus builds stronger defence”;, accessed 20 October 2007.

465 ^ 3.3.18 | 4.3.5    Fowke et al. “Resistance to HIV-1 infection among persistently seronegative prostitutes in Nairobi, Kenya”, Lancet, 348 (1996) 1347-51.

466^  Kaul et al., “CD8(+) lymphocytes respond to different HIV epitopes in seronegative and infected subjects”, Journal of Clinical Investigation, 107 (2001) 1303-10.

467^  Kaul et al., “HIV-1 Env-specific cytotoxic T-lymphocyte responses in exposed, uninfected Kenyan sex workers: a prospective analysis”, AIDS, 18 (2004) 2087-9.

468^  McNicholl & Promadej, “Insights into the role of host genetic and T-cell factors in resistance to HIV transmission from studies of highly HIV-exposed Thais”, Immunologic Research, 29 (2004) 161-74.

469^  Goh et al., “Protection against human immunodeficiency virus type 1 infection in persons with repeated exposure: evidence for T cell immunity in the absence of inherited CCR5 coreceptor defects”, Journal of Infectious Diseases, 179 (1999) 548-57.

470^  Farquhar et al., “Human leukocyte antigen (HLA) B*18 and protection against mother-to-child HIV type 1 transmission”, AIDS Research & Human Retroviruses, 20 (2004) 692-7.

471^  Kuhn et al., “T-helper cell responses to HIV envelope peptides in cord blood: protection against intrapartum and breast-feeding transmission”, AIDS, 15 (2001) 1-9.

472^  Clerici et al., “HIV-specific T-helper activity in seronegative health care workers exposed to contaminated blood”, JAMA, 271 (1992) 42-6.

473^  Pinto et al., “ENV-specific cytotoxic T lymphocyte responses in HIV seronegative health care workers occupationally exposed to HIV-contaminated body fluids”, Journal of Clinical Investigation, 96 (1995) 867-76.

474^  Makedonas et al., “HIV-specific CD8 T-cell activity in uninfected injection drug users is associated with maintenance of seronegativity”, AIDS, 16 (2002) 1595-1602.

475^  Barretina et al., “Evaluation of the putative role of C–C chemokines as protective factors of HIV-1 infection in seronegative hemophiliacs exposed to contaminated hemoderivatives”, Transfusion, 40 (2000) 461-7.

476^  William Langley, “The search for Salome's secret”, The Telegraph (UK), 17 April 2006;

477^  Donald G. McNeil Jr., “Anti-H.I.V. trial in Africa canceled over failure to prevent infection”, New York Times, 26 November 2011, p. A6.

478^  Harrison & Lamphear, “Microbicides”, in Mayer & Pizer (eds.), The AIDS Pandemic: Impact on Science and Society (Elsevier Academic Press, 2005) pp. 190-235.

479^  “Newer approaches to HIV prevention [Editorial]”, Lancet, 369 (2007) 615.

480^  Nayanah Siva, “Cash infusion for HIV microbicides”, Nature Biotechnology, 27 (2009) 401-2.

481^  "Trial Shows Anti-HIV Microbicide Is Safe, but Does Not Prove It Effective", Population Council, 18 February 2008.

482 ^ 4.4.1 | 4.7.16    Henry H. Bauer, “‘HIV disease’ is not an illness”,

483 ^ 4.4.1 | 4.7.16    Henry H. Bauer, “No HIV ‘latent period’: dotting i’s and crossing t’s”,

484^  SEER Cancer Statistics Review, National Cancer Institute;

485^  Kemény et al., “Human herpesvirus 8 in classic Kaposi sarcoma”, Acta Microbiologica et Immunologica Hungarica, 43 (1996) 391-5.

486^  Boshoff & Chang, “Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus”, Annual Review of Medicine, 52 (2001) 453-70.

487^  T. F. Schulz, “KSHV (HHV8) infection”, Journal of Infection, 41 (2000) 125-9.

488^  Feller et al., “The prognostic significance of facial lymphoedema in HIV-seropositive subjects with Kaposi sarcoma”, AIDS Research and Therapy, 5 (2008) 2;

489 ^ 4.4.3 | 4.7.11    Centers for Disease Control and Prevention, “AIDS cases by year of diagnosis and definition category, diagnosed through December 1993, United States”, HIV/AIDS Surveillance Report, 5 (#4, 1994) p. 15, Table 11.

490 ^ 4.4.3 |    "A snapshot of cervical cancer", National Cancer Institute (updated November 2014).

491^  National Cancer Institute, SEER Cancer Statistics Review 1975-2003, Table V-1.

492^   Cox & Bruce, “Why are so many mid-life gay men getting HIV?”, Gay News, 15 March 2007; or

493^  Henry H. Bauer, “CD4 counts don’t count — OFFICIAL!”,

494^  Henry H. Bauer, “Italian analysis of HIV/AIDS data”,

495^  Henry H. Bauer, “What do CD4 counts mean?”,

496^  Hellerstein et al., “Directly measured kinetics of circulating T lymphocytes in normal and HIV-1- infected humans”, Nature Medicine, 5 (1999) 83-9 (see Fig. 4b).

497^  Henry H. Bauer, “HIV ‘infection’ disappears spontaneously”,

498^  Henry H. Bauer, “Another striking success against HIV/AIDS in Africa”,

499^  Henry H. Bauer, “HIV-positive babies are not virus-infected”,

500^  Henry H. Bauer, “Update: More spontaneous seroreversion”,

501^  Henry H. Bauer, “Noteworthy successes against AIDS in Africa”,

502^  Farzadegan et al., “Loss of human immunodeficiency virus type 1 (HIV-1) antibodies with evidence of viral infection in asymptomatic homosexual men. A report from the Multicenter AIDS Cohort Study”, Annals of Internal Medicine, 108 (1988) 785-90.

503^  Des Jarlais et al., “CD4 lymphocytopenia among injecting drug users in New York City”, Journal of Acquired Immune Deficiency Syndromes, 6 (1993) 820-2.

504^  Nicolosi et al., “Incidence and risk factors of HIV infection: a prospective study of seronegative drug users from Milan and northern Italy, 1987-1989”, Epidemiology, 1 (1990) 453-9.

505^  Ho et al., “Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection”, Nature, 373 (1995) 123-6.

506^  Wei et al., “Viral dynamics in human immunodeficiency virus type 1 infection”, Nature, 373 (1995) 117-22.

507^  Mark Craddock, “HIV: Science by press conference”, pp. 127-30 in AIDS: Virus or Drug-Induced?, P. H. Duesberg (ed.) (Kluwer, 1996).

508^  M. Roederer, “Getting to the HAART of T cell dynamics”, Nature Medicine, 4 (1998) 145-6.

509^  Duesberg & Bialy, “Duesberg and the right of reply according to Maddox-Nature”, pp. 241-70 in AIDS: Virus or Drug-Induced?, P. H. Duesberg (ed.) (Kluwer, 1996).

510^  Yates et al., “Understanding the slow depletion of memory CD4+ T cells in HIV infection”, PLoS Medicine, 4 (2007) e177.

511^  Henry H. Bauer, “Pick a number — pick **any** number”;

512^  Henry H. Bauer, “HIV/AIDS: Numbers that don’t add up”;


514 ^   "Confession of an 'AIDS Denialist': How I became a crank because we're being lied to about HIV/AIDS”, pp. 278-82 in You Are STILL Being Lied To: The REMIXED Disinformation Guide to Media Distortion, Historical Whitewashes and Cultural Myths, ed. Russ Kick (The Disinformation Company, 2009);

515^  R. Brookmeyer, “Reconstruction and future trends of the AIDS epidemic in the United States”, Science, 253 (1991) 37-42.

516^  Rosenberg et al., “Estimating HIV prevalence and projecting AIDS incidence in the United States: a model that accounts for therapy and changes in the surveillance definition of AIDS”, Statistics in Medicine, 11 (1992) 1633-55.

517^  Rian Malan, “AIDS in Africa: In search of the truth”, Rolling Stone Magazine, 22 November 2001.

518^  Rian Malan, “Africa isn’t dying of Aids”, The Spectator (London), 14 December 2003.

519^  Craig Timberg, “U.N. to cut estimate of AIDS epidemic — Population with virus overstated by millions”, Washington Post Foreign Service, 20 November 2007.

520^  Henry H. Bauer, “CDC versus CDC: Which data to believe?”,

521^  Henry H. Bauer, “CDC: lying via statistics”,

522^  Henry H. Bauer, “‘HIV/AIDS’ deaths: often not from ‘HIV’ nor from ‘AIDS’!”,

523 ^ 4.5.5 | |    Nicoli Nattrass, Mortal Combat: AIDS Denialism and the Fight for Antiretrovirals in Suth Africa (University of KwaZlu-Natal Province, 2007).

524 ^ 4.5.5 | |    Nicoli Nattrass, “AIDS and the scientific governance of medicine in post-apartheid South Africa”, African Affairs”, 107 (2008) 157-76.

525 ^ 4.5.5 |    Chigwedere et al., “Estimating the lost benefits of antiretroviral drug use in South Africa”, JAIDS, 49 (2008) 410-5.

526^  Henry H. Bauer, “Peer review and consensus (Scientific literacy, lesson 2)”, 4 January 2013,

527^  “HIV serious, unique challenge for Pakistan: Crocker”, 2 December 2006;

528^  “HIV rates lower than feared”, 27 August 2007, UN Integrated Regional Information Networks;, accessed 28 August 2007.

529^  Henry H. Bauer, “Spontaneous generation of ‘HIV’”,

530^  Henry H. Bauer, “Circumcision and condom idiocies”,

531^  Bailey et al., “Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial”, Lancet, 369 (2007) 643-56.

532^  Newell & Bärnighausen, “Male circumcision to cut HIV risk in the general population”, Lancet, 369 (2007) 617-8.

533^  Boyle & Hill, “Sub-Saharah African randomised clinical trials into male circumcision and HIV transmission: Methodological, ethical and legal concerns”, Journal of Law and Medicine, 19 (2011) 316-34.

534^  Auvert et al., “Randomized, controlled intervention trial of male circumcision for reduction of HIV infection risk: The ANRS 1265 trial”, PLoS Medicine, 2 (2005) e298.

535^  Halperin et al., [correspondence], AIDS, 16 (2002) 810-2.

536^  Millett et al., “Circumcision status and HIV infection among Black and Latino men who have sex with men in 3 US cities”, Journal of Acquired Immune Deficiency Syndromes, 46 (2007) 643-50.

537^  Millett et al., “Circumcision status and risk of HIV and sexually transmitted infections among men who have sex with men: A meta-analysis”, JAMA, 300 (2008) 1674-84.

538^  Gray et al., “Male circumcision and HIV acquisition and transmission: cohort studies in Rakai, Uganda”, AIDS, 14 (2000) 2371-81.

539^  Michel Garenne, “Long-term population effect of male circumcision in generalised HIV epidemics in sub-Saharan Africa”, African Journal of AIDS Research, 7(2008) 1-8.

540^  Templeton et al., “Male circumcision to reduce the risk of HIV and sexually transmitted infections among men who have sex with men”, Current Opinion in Infectious Diseases, 23 (2010) 45-52.

541^  Green et al., “Male circumcision is not the HIV ‘vaccine’ we have been waiting for!”, Future HIV Therapy, 2 (2008) 193-9.

542^  Weiss et al., “Male circumcision and risk of HIV infection in sub-Saharan Africa: a systematic review and meta-analysis”, AIDS, 14 (2000) 2361-70.

543^  Potterat et al., “The protective effect of male circumcision as a faith lift for the troubled paradigm of HIV epidemiology in sub-Saharan Africa”, PLoS Medicine, 3 (2006) e64; author reply e67.

544^  Gray et al., “Male circumcision for HIV prevention in men in Rakai, Uganda: a randomised trial”, Lancet, 369 (2007) 657-66.

545^  Brewer et al., “Male and female circumcision associated with prevalent HIV infection in virgins and adolescents in Kenya, Lesotho, and Tanzania”, Annals of Epidemiology, 17 (2007) 217-26.

546^  “Zimbabwe targets on single digit HIV prevalence”, 14 September 2006;

547^  Peter Matambanadzo, “Country leads SADC in reducing HIV prevalence, incidence”, Herald (Harare), 22 November 2007;

548^  Caesar Zvayi, “Decline in HIV prevalence should inspire other sectors”, The Herald (Harare), 8 September 2006;, accessed 8 September 2006.

549^  Steve Berry & Rob Noble, “Why is Uganada interesting?”, (broken link),7 February 2008;

550^  Richard & Rosalind Chirimuuta, AIDS, Africa and Racism (Free Association Books [London, UK], 1989).

551^  J. M. Klopper, “AIDS — report of an epidemiological seminar”, South African Medical Journal, 68 (1985) 617-8.

552^  Lyons et al., “Lack of evidence of HTLV-III endemicity in southern Africa”, New England Journal of Medicine, 312(1985) 1257-8.

553^  Batungwanayo et al., “Pulmonary disease associated with the human immunodeficiency virus in Kigali, Rwanda. A fiberoptic bronchoscopic study of 111 cases of undetermined etiology”, American Journal of Respiratory and Critical Care Medicine, 149 (1994) 1591-6.

554^  Central African Journal of Medicine 1999, 45:127-8

555^  Henry H. Bauer, “Cocaine and heroin aren’t good for you! [a Golden Fleece Award]”,

556^  Henry H. Bauer, “Crack cocaine causes AIDS!”,

557^  Henry H. Bauer, “HIV/AIDS illustrates cognitive dissonance”,

558^  Henry H. Bauer, “Estonian drug addicts don’t have much sex”,

559^  Henry H. Bauer, “‘HIV/AIDS’ in Estonia: Demographics and shibboleths”,

560^  Henry H. Bauer, “Least susceptible = most affected?! More HIV/AIDS nonsense”,

561^  Theo Smart, “Structural Factors — PEPFAR: Greater wealth, not poverty, associated with higher HIV prevalence in Africa, according to survey”, nam-aidsmap, 2 August 2006;

562^  Henry H. Bauer, “HIV: It must have been transmitted by bite!”,

563^  Henry H. Bauer, “Babies infect mothers; crazy theory ruins lives”,

564^  Henry H. Bauer, “Is tuberculosis an aphrodisiac?”,

565^  Quentin Casey, “Obesity problem grows with HIV crisis: Being heavy seen as sign of health in hard- hit country”, National Post [Canada], 19 August 2006;

566^  Joe De Capua, "Malnutrition worsens the HIV/AIDS pandemic", Voice of America, 1 November 2009.

567^  Lawrence K. Altman, “Washing after sex may raise H.I.V. risk”, New York Times, 21 August 2007;

568^  Shelburne et al., “Immune Reconstitution Inflammatory Syndrome: Emergence of a unique syndrome during Highly Active Antiretroviral Therapy”, Medicine, 81 (2002) 213-27.

569^  Henry H. Bauer, “Compounding HIV/AIDS absurdities”,

570^  “World AIDS Day — December 1, 2007”, MMWR, 56 (#47, 2007) 1233.

571^  MacKellar et al., “Unrecognized HIV infection, risk behaviors, and perceptions of risk among young men who have sex with men opportunities for advancing HIV prevention in the third decade of HIV/AIDS”, Journal of Acquired Immune Deficiency Syndromes, 38 (2005) 603-14.

572^  “Unrecognized HIV infection, risk behaviors, and perceptions of risk among young black men who have sex with men — Six U.S. cities, 1994-1998”, MMWR, 51 (#33, 2002) 733-6;

573^  Michael Carter, “HIV testing in gay social venues is viewed as inappropriate”, 22 January 2007;

574^  Judith Duffy, “33% with HIV in UK don't know they're infected”, Sunday Herald (Scotland), 29 April 2007;

575^  Hall et al., “Estimation of HIV Incidence in the United States”, JAMA, 300 (2008) 520-9.

576^  Centers for Disease Control & Prevention, “HIV in the United States: At A Glance”,

577^  Moss et al., “Suppression of human immunodeficiency virus replication during acute measles”, Journal of Infectious Diseases,185 (2002) 1035-42.

578^  Grivel et al.., “Inhibition of HIV-1 replication in human lymphoid tissues ex vivo by measles virus”, Journal of Infectious Diseases,192 (2005) 71-8.

579^  García et al., “In vitro suppression of human immunodeficiency virus type 1 replication by measles virus”, Journal of Virology, 79 (2005) 9197-205.

580^  García et al., “Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes”, Journal of General Virology, 89 (2008) 984-93.

581^  Moss et al., “Suppression of human immunodeficiency virus type 1 viral load during acute measles”, Pediatric Infectious Disease Journal,28 (2009) 63-5.

582^  “Medical Services completes testing of VScan HIV test kit with exceptional results”, AIDS Weekly, 22 January 2007.

583^  Saberi et al., “Quality of sleep: Associations with antiretroviral nonadherence”, AIDS Patient Care and STDs, 25 (2011) 517-24.

584^  Henry H. Bauer, “What HIV drugs do”,

585^  Henry H. Bauer, “The ‘science’ of AIDS”,

586^  Henry H. Bauer, “Prediction: What antiretroviral drugs will accomplish”,

587^  Henry H. Bauer, “How antiretroviral drugs are approved”,

588^  Volberding & Deeks, “Antiretroviral therapy and management of HIV infection”, Lancet, 376 (2010) 49-62.

589 ^ 5.1 | 7.1.3    Dore & Cooper, “HAART's first decade: success brings further challenges”, Lancet, 368 (2006) 427- 8.

590^  Antiretroviral Therapy (ART) Cohort Collaboration”, HIV treatment response and prognosis in Europe and North America in the first decade of highly active antiretroviral therapy: a collaborative analysis”, Lancet, 368 (2006) 451-8.

591^  Van Benthem et al., “Is AIDS a floating point between HIV seroconversion and death? Insights from the Tricontinental Seroconverter Study”, AIDS, 12 (1998) 1039-45.

592^  Henry H. Bauer, “Death, antiretroviral drugs, and cognitive dissonance”,

593^  Henry H. Bauer, “Antiretroviral therapy has saved 3 million life-years”,

594^  Henry H. Bauer, “HIV/AIDS scam: Have antiretroviral drugs saved 3 million life-years?”,

595^  Henry H. Bauer, “Antiretroviral treatment benefits? From 3 million to 1.2 million to …!?!”,

596^  Henry H. Bauer, “AIDS deaths: owing to antiretroviral drugs or to lack of antiretroviral treatment?”,

597^  Henry H. Bauer, “Living with HIV; dying from what?”,

598^  D. Josefson, “FDA warning to manufacturers of AIDS drugs”, British Medical Journal, 322 (2001) 1143.

599^  Kallen et al., “Direct-To-Consumer Advertisements For HIV Antiretroviral Medications: A Progress Report — Certain omissions in these ads do not technically violate current FDA regulations, but they do violate those regulations' intent”, Market Watch, September/October 2007, 1392-8.

600^  Daryl Lindsey, “The ‘Joe Camel’ ads of AIDS? The FDA says ads for drugs to suppress HIV are making false promises, and could be contributing to an epidemic of unsafe sex”,, 8 May 2001;

601^  The Antiretroviral Therapy (ART) Cohort Collaboration, “HIV treatment response and prognosis in Europe and North America in the fi rst decade of highly active antiretroviral therapy: a collaborative analysis”, Lancet, 368 (2006) 451-8 .

602^  Van Sighem et al., “Mortality in patients with successful initial response to Highly Active Antiretroviral Therapy is still higher than in non–HIV-Infected individuals”, Journal of Acquired Immune Deficiency Syndromes, 40 (2005) 212-8.

603^  Walensky et al., “The survival benefits of AIDS treatment in the United States”, Journal of Infectious Diseases, 194 (2006) 11-9.

604 ^ 5.1.4 | 5.1.6    Centers for Disease Control & Prevention, “Deaths among Persons with AIDS through December 2000”, HIV/AIDS Surveillance Supplemental Rppoert, 8 (#1, 2002).

605^  Centers for Disease Control & Prevention, “Management of possible sexual, injecting-drug–use, or other nonoccupational exposure to HIV, including considerations related to antiretroviral therapy — Public Health Service statement”, MMWR, 47 (RR17, 25 September 1998) 1-19.

606^  Fischl et al., “The efficacy of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial”, New England Journal of Medicine, 317 (1987) 185-91.

607 ^ 5.2.3 | | | |    Richman et al., “The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial”, New England Journal of Medicine, 317 (1987) 192-7.

608^  J. A. Sonnabend, “Review of AZT multicenter trial data”, October 1987;

609^  J. A. Sonnabend, “AZT: The Clinical Trial that led to its approval”, 28 January 2011;

610^  John Lauritsen, Poison By Prescription (ASKLEPIOS, 1990, ISBN 0-943742-06-4).

611^  “Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee”, Lancet, 343 (1994) 871-81.

612^  “Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents — What Not to Use”, NIH AIDSinfo, Clinical Guidelines Portal, 27 March 2012;

613 ^ | 5.2.6 | |    Walker & Poirier, “Special Issue on Health Risks of Perinatal Exposure to Nucleoside Reverse Transcriptase Inhibitors”, Environmental and Molecular Mutagenesis, 48 (2007) 159-65.

614^  Borojerdi et al., “Centrosomal amplification and aneuploidy induced by the antiretroviral drug AZT in hamster and human cells”, Mutation Research, 665 (2009) 67-74.

615^  Papadopulos-Eleopulos et al., “A critical analysis of the pharmacology of AZT and its use in AIDS”, Current Medical Research & Opinion,15 (suppl. 1, 1999) s1-45.

616^  NIH Treatment Guidleines, 12 February 2013, p. F5.

617 ^ 5.2.6 |    Kohler & Lewis, “Review Article: A brief overview of mechanisms of mitochondrial toxicity from NRTIs”, Environmental and Molecular Mutagenesis, 48 (2007) 166-72.

618^  Treatment Guidleines, 12 February 2013, p. F15.

619^  GlaxoSmithKline, “Pr RETROVIR(AZT™)”, revised 21 September 2005.

620^  David Crowe, “Concerns about HAART — Highly Active Anti-Retroviral Therapy”, June 2001,

621^  Fellay et al., “Prevalence of adverse events associated with potent antiretroviral treatment: Swiss HIV Cohort Study”, Lancet, 358 (2001) 1322-7.

622^  Panilio et al., “Updated U.S. Public Health Service Guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis”, MMWR, 54 (RR09, 30 September 2005) 1-17.

623^  Press release, 5 February 2001; “Anti-HIV/AIDS drugs — New US guidelines make the case for ongoing scientific inquiry . . . . serious toxicities are associated with long-term use of anti-retroviral drugs””, ANC Today, 20 April 2001;

624^  Reisler et al., “Grade 4 events are as important as AIDS events in the era of HAART”, Journal of Acquired Immune Deficiency Syndromes, 34 (2003) 379-86.

625^  Fauci & Whitescarver, “The 30th Anniversary of the First Reported Cases of AIDS”, NIH Medline Plus, 6 (2011) 10-2;

626^  Pujades-Rodríguez et al., “Toxicity associated with Stavudine dose reduction from 40 to 30 mg in first-line antiretroviral therapy”, PLoS ONE, 6 (2011) e28112.

627^  Isabelle Andrieux-Meyer, Médecins Sans Frontières, et al., to Bill & Melinda Gates Foundation, 14 December 2011.

628^  Henry H. Bauer, “HAART? You’ve got to be crazy . . .”,

629^  Henry H. Bauer, “Drug non-adherence, imaginary epidemics, and sexual nonsense”,

630^  Henry H. Bauer, “Avoiding life-saving treatment”,

631^  Henry H. Bauer, “Platinum Fleecing and the HIV/AIDS Industry”,

632^  Onnie Mary Phuthe, “A scar means, I survived”.

633^  Rosen et al., (2007) “Patient retention in antiretroviral therapy programs in Sub-Saharan Africa: A systematic review”, PLoS Medicine, 4 (2007) e298;

634^  Cohen et al., “Medically eligible women who do not use HAART: the importance of abuse, drug use, and race”, American Journal of Public Health, 94 (2004) 1147-51.

635^  Pp. K1-6 and passim in Guidelines for the Use of Antiretroviral Agents inHIV-1-Infected Adults and Adolescents,14 July 2013; and passim in all earlier versions.

636^  P. K7 in Guidelines for the Use of Antiretroviral Agents inHIV-1-Infected Adults and Adolescents,14 July 2013 .

637^  Clinical trial NCT00068809, “4-Day-A-Week Treatment Plan for HIV Infected Adolescents”;

638^  David France, “Another Kind of AIDS Crisis”, New York, 1 November 2009;

639^  Jane Gross, “AIDS patients face downside of living longer”, New York Times, 6 January 2008;, accessed 4 August 2013.

640 ^   Lewis & Dalakas, “ Mitochondrial toxicity of antiviral drugs”, Nature Medicine, 1 (1995) 417-22.

641^  Benhammou et al., “Clinical mitochondrial dysfunction in uninfected children born to HIV-infected mothers following perinatal exposure to nucleoside analogues”, Environmental and Molecular Mutagenesis, 48 (2007) 173-8.

642^  Chan et al., “Mitochondrial toxicity in hearts of CD-1 mice following perinatal exposure to AZT, 3TC, or AZT/3TC in combination”, Environmental and Molecular Mutagenesis, 48 (2007) 190-200.

643^  Divi et al., “Morphological and molecular course of mitochondrial pathology in cultured human cells exposed long-term to Zidovudine”, Environmental and Molecular Mutagenesis, 48 (2007) 179-89.

644^  Divi et al., “Transplacentally exposed human and monkey newborn infants show similar evidence of nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity”, Environmental and Molecular Mutagenesis, 48 (2007) 201-9.

645^  Blanche et al., “Persistent mitochondrial dysfunction and perinatal exposure to antiretroviral nucleoside analogues”, Lancet, 354 (1999) 1084-9.

646^  Payne et al., “Mitochondrial aging is accelerated by anti-retroviral therapy through the clonal expansion of mtDNA mutations”, Nature Genetics, 43 (2011) 806-10.

647^  Saitoh et al., “Impact of nucleoside reverse transcriptase inhibitors on mitochondria in Human Immunodeficiency Virus Type 1-infected children receiving Highly Active Antiretroviral Therapy”, Antimicrobial Agents and Chemotherapy,51 (2007) 4236-42.

648 ^   Seth Roberts, “Lab Rat”, Spy, July 1990, pp. 70-9;;

649^  Arnaudo et al., “Depletion of muscle mitochondrial DNA in AIDS patients with zidovudine-induced myopathy”, Lancet, 337 (1991) 508-10.

650^  Benbrik et al., “Cellular and mitochondrial toxicity of zidovudine (AZT), didanosine (ddI) and zalciltabine (ddC) on cultured human muscle cells”, Journal of Neurological Sciences, 149 (1997) 19- 25.

651^  Barret et al., “Persistent mitochondrial dysfunction in HIV-1-exposed but uninfected infants: clinical screening in a large prospective cohort”, AIDS, 17 (2003) 1769-85.

652^  Henry H. Bauer, “Protease inhibitors cause oxidative stress”,

653^  Henry H. Bauer, “Nevirapine, TB, and HIV/AIDS”,

654^  Henry H. Bauer, “Nevirapine — P.S.”,

655 ^ | | | | | | | | |    NIH AIDSinfo, “Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents”, 14 July 2013, Table 13, pp. K8-12.

656^  Henry H. Bauer, “State of HIV/AIDS denial: Carcinogenic HAART”,

657^  Gerald N. Wogan, “Does perinatal antiretroviral therapy create an iatrogenic cancer risk?”, Environmental and Molecular Mutagenesis,48 (2007) 210-4.

658^  Ofelia A. Olivero, “Mechanisms of genotoxicity of nucleoside reverse transcriptase inhibitors”, Environmental and Molecular Mutagenesis,48 (2007) 215-23.

659^  Torres et al., “Mutagenicity of zidovudine, lamivudine, and abacavir following in vitro exposure of human lymphoblastoid cells or in utero exposure of CD-1 mice to single agents or drug combinations”, Environmental and Molecular Mutagenesis, 48 (2007) 224-38.

660^  Meng et al., “Plasma and cellular markers of 3-azido-3-dideoxythymidine (AZT) metabolism as indicators of DNA damage in cord blood mononuclear cells from infants receiving prepartum NRTIs”, Environmental and Molecular Mutagenesis, 48 (2007) 307-21.

661^  Walker et al., “Transplacental carcinogenicity of 3-azido-3-deoxythymidine in B6C3F1 mice and F344 rats”, Environmental and Molecular Mutagenesis, 48 (2007) 283-98.

662^  Escobar et al., “Genotoxicity assessed by the Comet and GPA assays following in vitro exposure of human lymphoblastoid cells (H9) or perinatal exposure of mother-child pairs to AZT or AZT-3TC”, Environmental and Molecular Mutagenesis,48 (2007) 330-43.

663^  Witt et al., “Elevated frequencies of micronucleated erythrocytes in infants exposed to zidovudine in utero and postpartum to prevent mother-to-child transmission of HIV”, Environmental and Molecular Mutagenesis, 48 (2007) 322-9.

664^  Carter et al., “Relative mutagenic potencies of several nucleoside analogs, alone or in drug pairs, at the HPRT and TK loci of human TK6 lymphoblastoid cells”, Environmental and Molecular Mutagenesis, 48 (2007) 239-47.

665^  Jan Wise et al., “Neuropsychiatric complications of nevirapine treatment”, British Medical Journal, 324 (2002) 879.

666^  Morlese et al., “Nevirapine-induced neuropsychiatric complications, a class effect of non-nucleoside reverse transcriptase inhibitors?”, AIDS, 16 (2002) 1840-1.

667^  Arendt et al., “Neuropsychiatric side effects of efavirenz therapy”, Expert Opinion on Drug Safety, 6 (2007) 147-54.

668^  Call et al., “The changing etiology of chronic diarrhea in HIV-infected patients with CD4 cell counts less than 200 cells/mm3”, American Journal of Gastroenterology, 95 (2000) 3142-6.

669^  Rufo et al., “Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl-secretion by T84 cells via prolongation of cytosolic Ca2+ signaling”, American Journal of Physiology. Cell Physiology, 2004 286 (2004) C998-1008.

670^  Wand et al., “Metabolic syndrome, cardiovascular disease and type 2 diabetes mellitus after initiation of antiretroviral therapy in HIV infection”, AIDS, 21 (2007) 2445-53.

671^  Lanzafame et al., “Antiretroviral Therapy-associated diseases are common in the long-term”, AIDS Research and Human Retroviruses, 27 (2011) 931-2.

672 ^   Carr et al., “A syndrome of peripheral lipodystrophy, hyperlipidaemia and insulin resistance in patients receiving HIV protease inhibitors”, AIDS, 12 (1998) F51-8.

673 ^ |    K. Samaras, “The burden of diabetes and hyperlipidemia in treated HIV infection and approaches for cardiometabolic care”, Current HIV/AIDS Reports, 9 (2012) 206-17.

674^  Carr et al., “Pathogenesis of HIV-1-protease inhibitor-associated peripheral lipodystrophy, hyperlipidaemia, and insulin resistance”, Lancet, 351 (1998) 1881-3.

675^  Gan et al., “Altered myocellular and abdominal fat partitioning predict disturbance in insulin action in HIV protease inhibitor-related lipodystrophy”, Diabetes, 51 (2002) 3163-9.

676^  Carr et al., “Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study”, Lancet, 353 (1999) 2093-9.

677^  Bradbury & Samaras, “Antiretroviral therapy and the human immunodeficiency virus--improved survival but at what cost?”, Diabetes, Obesity & Metabolism, 10 (2008) 441-50.

678 ^ |    K. Samaras, “Metabolic consequences and therapeutic options in highly active antiretroviral therapy in human immunodeficiency virus-1 infection”, Journal of Antimicrobial Chemotherapy, 61 (2008) 238-45.

679^  K. Samaras, “Prevalence and pathogenesis of diabetes mellitus in HIV-1 infection treated with combined antiretroviral therapy”, Journal of Acquired Immune Deficiency Syndromes, 50 (2009) 499- 505.

680^  Murata et al., “The mechanism of insulin resistance caused by HIV protease inhibitor therapy”, Journal of Biological Chemistry,275 (2000) 20251-4.

681^  Samaras et al., “Postprandial lipid effects of low-dose ritonavir vs. raltegravir in HIV-uninfected adults”, AIDS, 24 (2010) 1727-31.

682^  C. J. Cohen, “Ritonavir-boosted protease inhibitors, Part 2: cardiac implications of lipid alterations”, AIDS Reader, 15 (2005) 528-32, 537-8.

683^  Chuapai et al., “Lipodystrophy and dyslipidemia in human immunodeficiency virus-infected Thai patients receiving antiretroviral therapy”, Journal of the Medical Association of Thailand, 90 (2007) 452-8.

684^  Aurpibul et al.., “Lipodystrophy and metabolic changes in HIV-infected children on non-nucleoside reverse transcriptase inhibitor-based antiretroviral therapy”, Antiviral Therapy, 12 (2007) 1247-54.

685^  Chanu & Valensi, “Lipid disorders in patients with HIV-induced diseases” [in French], Presse Médicale, 34 (2005) 1087-94.

686^  Henry H. Bauer, “Misleading is worse than lying — The case of ‘HIV-associated’ lipodystrophy”,

687^  Puttawong et al., “Prevalence of lipodystrophy in Thai-HIV infected patients”, Journal of the Medical Association of Thailand, 87 (2004) 605-11.

688^  “HIV Protease Inhibitor drugs may adversely affect the scaffolding of the cell nucleus, study finds”, 20 July 2007;, referring to Coffinier et al., “HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cells”, Proceedings of the National Academy of Sciences USA, 104 (2007) 13432-7.

689^  “Weight gain in HIV patients a challenging problem”, 1 January 2007;

690 ^ |    Brinkman et al., “Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy”, Lancet, 354 (1999) 1112-5.

691^  Massip et al., “Lipodystrophia with proteases inhibitors in HIV patients”, Thérapie, 52 (1997) 615.

692^  “Abnormal fat distribution and use of protease inhibitors”, Lancet, 351 (1998) 1735-7, reports from Rebecca Wurtz, Carr et al., Ho et al.

693^  Babl et al., “Abnormal body-fat distribution in HIV-1-infected children on antiretrovirals”, Lancet, 353 (1999) 1243-4.

694^  Miller et al., “Visceral abdominal-fat accumulation associated with use of indinavir”, Lancet, 351 (1998) 871-5.

695^  Kelleher et al., “Dyslipidemia due to retroviral protease inhibitors”, Nature Medicine, 8 (2002) 308.

696^  Henry H. Bauer, “HAART kills hearts”,

697^  Henry H. Bauer, “HAART, heart disease, & lying with statistics”,

698^  Friis-Møller et al., “Combination antiretroviral therapy and the risk of myocardial infarction”, New England Journal of Medicine, 349 (2003) 1993-2003.

699^  Currier et al., “Coronary heart disease in HIV-infected individuals”, Journal of Acquired Immune Deficiency Syndromes, 33 (2003) 506-12.

700^  Mary-Krause et al.., “Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men”, AIDS, 17 (2003) 2479-86.

701^  McKee et al., “Phosphorylation of thymidine and AZT in heart mitochondria: Elucidation of a novel mechanism of AZT cardiotoxicity”, Cardiovascular Toxicology, 4 (2004) 155-67.

702^  “FDA to review safety of GSK, BMS antiretrovirals Abacavir, Didanosine”, Kaiser Health News, 28 March 2008;

703^  Writing Committee of the D:A:D: Study Group, “Cardio- and cerebrovascular events in HIV-infected persons”, AIDS, 18 (2004) 1811-7.

704^  Jericó et al., “Subclinical carotid atherosclerosis in HIV-infected patients — Role of Combination Antiretroviral Therapy”, Stroke, 37 (2006) 812-7.

705^  Strategies for Management of Anti-Retroviral Therapy/INSIGHT; DAD Study Groups, “Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients”, AIDS, 22 (2008) F17-24.

706^  Lai et al., “Long-term Combination Antiretroviral Therapy is associated with the risk of coronary plaques in African Americans with HIV infection”, AIDS Patient Care and STDs, 23 (2009) 815-24.

707^  Henry H. Bauer, “Kidney-disease denialism (a special case of HAART denialism)”,

708^  Labarga et al., “Kidney tubular abnormalities in the absence of impaired glomerular function in HIV patients treated with tenofovir”, AIDS, 23 (2009) 689-96.

709^  Wever et al., “Incomplete reversibility of Tenofovir-related renal toxicity in HIV-infected men”, Journal of Acquired Immune Deficiency Syndromes,55 (2010) 78-81.

710^  Mocroft et al., “Estimated glomerular filtration rate, chronic kidney disease and antiretroviral drug use in HIV-positive patients”, AIDS, 24 (2010) 1667-78.

711^  Hitti et al., “Maternal toxicity with continuous nevirapine in pregnancy: results from PACTG 1022”, Journal of Acquired Immune Deficiency Syndromes,36 (2004) 772-6.

712^  Celia Farber, “Out Of Control: AIDS and the corruption of medical science”, Harper’s, 1 March 2006; Chapter 12 in 11;

713^  “Poisoning African mothers”,;

714^  Amy Justice, 14th International AIDS Conference, Barcelona, July 2002;

715^  Servoss et al., “Predictors of antiretroviral-related hepatotoxicity in the adult AIDS Clinical Trial Group (1989–1999)”, Journal of Acquired Immune Deficiency Syndromes, 43 (2006) 320-3.

716^  “FDA issues alert about HIV drug Prezista”, 24 March 2008;, accessed 2 April 2008.

717^  Phadke et al., “Nevirapine to prevent HIV transmission via breastfeeding”, Lancet, 372 (2008) 287.

718^  Moore et al., “Incidence of pancreatitis in HIV-infected patients receiving nucleoside reverse transcriptase inhibitor drugs”, AIDS, 15 (2001) 617-20.

719^  Henry H. Bauer, “HAART causes strokes”,

720^  Bonjoch et al., “High prevalence of and progression to low bone mineral density in HIV-infected patients: a longitudinal cohort study”, AIDS, 24 (2010) 2827-33.

721^  Brown & Qaqish, “Antiretroviral therapy and the prevalence of osteopenia and osteoporosis: a meta- analytic review”, AIDS, 20 (2006) 2165-74.

722^  Day & Lewis, “Oxidative Stress in NRTI-Induced Toxicity: Evidence From Clinical Experience and Experiments In Vitro and In Vivo”, Cardiovascular Toxicology, 4 (2004) 207-16.

723^  Estaquier et al., “Effects of antiretroviral drugs on human immunodeficiency virus type 1-induced CD4(+) T-cell death”, Journal of Virology, 76 (2002) 5966-73.


725^  Henry H. Bauer, “Best treatment for HIV: This year’s advice, last year’s, or next year’s?”,

726^  Henry H. Bauer, “Antiretroviral drugs: History and rhetoric”,

727^  Henry H. Bauer, “Official guidelines for HIV treatment”,

728^  “Antiretroviral regimens or components that should not be offered at any time”, Tables on pp. G3-4 in the Treatment Guidelines version downloaded 14 July 2013.

729^  Henry H. Bauer, “Antiretroviral drugs lead to normal life?”

730^  Herzenberg et al., “Glutathione deficiency is associated with impaired survival in HIV disease”, Proceedings of the National Academy of Sciences USA, 94 (1997) 1967-72.

731^  Giraldo et al., “Treating and preventing AIDS — A guide to basic principles for effective, nontoxic and inexpensive alternatives”, February 2003;

732^  H. C. Greenspan, “The role of reactive oxygen species, antioxidants and phytopharmaceuticals in human immunodeficiency virus activity”, Medical Hypotheses, 40 (1993) 85-92.

733^  Henry H. Bauer, “AIDS as intestinal dysbiosis”,

734^  Henry H. Bauer, “Alternative treatments for AIDS”,

735 ^ 5.5.1 |    Henry H. Bauer, “AIDS as intestinal dysbiosis”, 23 February 2008;

736 ^ 5.5.2 |    Duesberg et al., “The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition”, Journal of Bioscience, 28 (2003) 383-412.

737^  Cassone et al., “In vitro and in vivo anticandidal activity of human immunodeficiency virus protease inhibitors”, Journal of Infectious Diseases, 180 (1999) 448-53.

738^  Atzori et al., “In vitro activity of human immunodeficiency virus protease inhibitors against Pneumocystis carinii”, Journal of Infectious Diseases, 181 (2000) 1629-34.

739^  Gigerenzer et al., “AIDS counselling for low-risk clients”, AIDS Care, 10 (1998) 197-211.

740^  Kalb & Murr, “Battling a black epidemic”, Newsweek, 15 May 2006, 42-8.

741^  For example, Andre Parenzee, See also many cases cited by the Office of Medical & Scientific Justice:,

742^  HIV Justice Network, 3 October 2012;

743^  “Woman with HIV gets 3 years for spitting in another woman's face”, Associated Press, 22 July 2008;

744^  Luke Darby, “HIV-positive man charged with aggravated assault for spitting on police officers”, Dallas Observer, 31 May 2013;

745 ^ | 6.2.2    Rachel Quigley, MailOnline, 2 September 2013;

746^  Eligon & Wilson, “Morrison says error in H.I.V. test hurt career”, New York Times, 22 July 2007;

747^  Fazlulhaq & Kaviratna, “HIV/AIDS-affected women take woes before ‘court’”, Sunday Times (Sri Lanka), 19 August 2007;

748^  Dignity Denied: Violations of the Rights of HIV-Positive Women in Chilean Health Facilities, Vivo Positivo (Chile) & Center for Reproductive Rights (USA), 2010;

749^  “AIDS tests on foster children violated rules”, Associated Press, 16 June 2005;

750^  “AIDS drugs tested on foster kids”, Associated Press, 11 February 2009;

751^  “Guinea Pig Kids”;

752^  Jamie Doran, “New York's HIV experiment”, 30 November 2004;

753^  “Guinea Pig Kids”, 29 November 2004;

754^  “Guinea Pig Kids: How New York City is using children to test experimental AIDS drugs”, 22 December 2004;

755^  Hallfors et al., “Sexual and drug behavior patterns and HIV and STD racial disparities: the need for new directions”, American Journal of Public Health, 97 (2007) 125-32.

756^  Elford et al., “Sexual behaviour of people living with HIV in London: implications for HIV transmission”, AIDS, 21 (suppl. 1, 2007) S63-70.

757^  “One-third of HIV-infected gay men have unsafe sex: CDC”, HealthDay News, 3 December 2007;

758^  Harawa et al., “Associations of race/ethnicity with HIV prevalence and HIV-related behaviors among young men who have sex with men in 7 urban centers in the United States”, Journal of Acquired Immune Deficiency Syndromes, 35 (2004) 526-36.

759^  Harawa et al., “Do differences in relationship and partner attributes explain disparities in sexually transmitted disease among young white and black women?”, Journal of Adolescent Health, 32 (2003) 187-91.

760^  Torian et al., “HIV infection in men who have sex with men, New York City Department of Health sexually transmitted disease clinics, 1990-1999: a decade of serosurveillance finds that racial disparities and associations between HIV and gonorrhea persist”, Sexually Transmitted Diseases, 29 (2002) 73-8.

761^  Aral et al., “Understanding and responding to disparities in HIV and other sexually transmitted infections in African Americans”, Lancet, 372 (2008) 337-40.

762^  Garnett & Johnson, “Coining a new term in epidemiology: concurrency and HIV”, AIDS, 11 (1997) 681-3.

763^  Morris & Kretzschmar, “Concurrent partnerships and the spread of HIV”, AIDS, 11 (1997) 641-8.

764^  “Change in sexual behaviors needed to curb spread of HIV in Africa, some health experts say”, Kaiser Health Network, 19 January 2007;

765^  “A proven strategy to fight HIV”, Boston Globe, 12 February 2008;

766^  Greg Millett (Epidemiology Branch, Division of HIV/AIDS Prevention, National Center of HIV/STD/TB Prevention), “The ‘Down Low’: More questions than answers”, PowerPoint presentation, 11th Conference on Retroviruses and Opportunistic Infections, February 2004 (San Francisco, CA); accessed 4 August 2013 via Google search.

767^  Millett et al., “Focusing “Down Low”: Bisexual black men, HIV risk and heterosexual transmission”, Journal of the National Medical Association,97 (2005) 52S-59S.

768^  Anne Harding, “‘Down low’ myth distorts HIV research, prevention”, Reuters Health, 28 February 2007; — Source: 769.

769^  Ford et al., “Black sexuality, social construction, and research targeting ‘The Down Low’ (‘The DL’)”, Annals of Epidemiology, 17 (2007) 209-16.

770^  Mark A. Weinberg, “We need to do a better job at public health if we are to limit the spread of HIV”, in Symposium: AIDS and Its Transmission, Globe and Mail, 6 September 2008; accessed 9 September 2008.

771^  Henry H. Bauer, “What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008;

772^  “Damages claimed for AIDS diagnosis”, New York Times, 26 October 1992;


774^  Henry H. Bauer, “A small hitch in the bandwagon?”,

775^  The Fair Allocation In Research Foundation (FAIR Foundation),

776^  Angela Pirisi, “Profile: Richard Darling, President and CEO of the FAIR Foundation”, Lancet, 364 (2004) 409.

777^  Piller & Smith, “A TIMES Investigation: Unintended victims of Gates Foundation generosity — Donations to fight AIDS, TB and malaria in Africa have inadvertently put many of those with other basic healthcare needs at risk”, Los Angeles Times, 16 December 2007;,0,3743924.story

778^  Jeremy Shiffman, “Has donor prioritization of HIV/AIDS displaced aid for other health issues?”, Health Policy and Planning, 23 (2008) 95-100;, accessed 23 February 2008.

779^  Maria Cheng, “Experts call for rethinking AIDS money — AIDS experts suggest some of their billions should be shifted to basic health problems”, Associated Press, 18 January 2008;

780^  Arango & Stelter, “Messages with a mission, embedded in TV shows”, New York Times, 2 April 2009, p. C1;, accessed 14 May 2009.

781^  Serge Lang, “HIV and AIDS: Questions of scientific and journalistic responsibility”, pp. 601-714 in Challenges (Springer, 1998).

782^  Henry H. Bauer, “Avoiding life-saving treatment”,

783^  Henry H. Bauer, “HAART makes things worse: Elsevier journal publishes HIV/AIDS heresies”,

784^  Henry H. Bauer, “HIV/AIDS grift”,

785^  Henry H. Bauer, “World AIDS Day: Black Stars and ‘life-saving’ HAART”,

786^  Henry H. Bauer, “HAART denialism, contd.”,

787^  Henry H. Bauer, “Hidden in plain sight: The damage done by antiretroviral drugs”,

788^  “Bioenergetic Therapy for Aging — Mitochondria hold the key to cellular life and death”, Life Extension Magazine, February 2001;

789^  Linnane et al., “Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases”, Lancet, 333 (1989) 642-5.

790^  Linnane et al., “Mitochondrial gene mutation: the ageing process and degenerative diseases”, Biochemistry International, 22 (1990) 1067-76;

791^  Rodney Shackelford, “The mitochondrial theory of aging”;

792^  Bratic & Larsson, “The role of mitochondria in aging”, Journal of Clinical Investigation, 123 (2013) 951-7.

793^  Neustadt & Pieczenik, “Medication-induced mitochondrial damage and disease”, Molecular Nutrition & Food Research, 52 (2008) 780-7.

794^  Bo-Mi Lim, “Korean soap opera tackles AIDS: TV show tells story of girl, 8, who is infected”, Associated Press, 16 May 2007;

795^  Valente & Bharath, “An evaluation of the use of drama to communicate HIV/AIDS information”, AIDS Education & Prevention, 11 (1999) 203-11.

796^  Soile Salo, HIV/AIDS and Educational Drama — Resource Material for Teachers Grades 4–12 (Ministyr of Basic education, Sport and Culture, Namibia, 2001).

797^  Magic Johnson on the Oprah Winfrey show, December 2005.

798^  Global AIDS Summit convened by former U.S. president Bill Clinton, CNN television, 29 April 2006, 8-9 p.m. EDT.

799^  Four-hour special FRONTLINE PBS television program, 30-31 May 2006.

800^  Television series Law and Order, re-broadcast 4 June 2004, 9 pm Eastern, USA cable.

801^  “Just one time. That’s all it took” — pp. 472-3 in Val McDermid, Beneath the Bleeding (2009).

802^  Detective Inspector John Rebus, in Ian Rankin, The Hanging Garden (1998).

803^  James Lee Burke, In the Electric Mist with Confederate Dead (Avon 1994) p. 251.

804^  P. 16 in in Val McDermid, Beneath the Bleeding, 2009.

805^  Daniel Easterman, Brotherhood of the Tomb (HarperPaperbacks, 1990) pp. 416-8.

806^  Henry H. Bauer, “Media: invariably wrong about HIV/AIDS”,

807^  Henry H. Bauer, “Real science isn’t news”, Science Writing Fellowships Program, Marine Biological Laboratory, Woods Hole (MA) 13 June 1996;

808^  The Media and HIV/AIDS: Making the Difference, Global Media AIDS Initiative (UNAIDS & Henry J. Kaiser Foundation, 2004).

809^  Obama orders stepped up effort against U.S. HIV/AIDS epidemic”, Yasmeen Abutaleb, Reuters, Washington, 15 July 2013.

810^  Henry H. Bauer, The Enigma of Loch Ness: Making Sense of a Mystery (University of Illinois Press, 1986) chapter 6.

811^  Henry H. Bauer, Science or Pseudoscience: Magnetic Healing, Psychic Phenomena, and Other Heterodoxies (University of Illinois Press, 2001) pp. 38-42, 154, 160-1.

812 ^ |    Papadopulos-Eleopulos et al., “The last debate”, Reappraising AIDS, December 1999;

813^  Tony Lance, “GRID = Gay Related Intestinal Dysbiosis? Explaining HIV/AIDS paradoxes in terms of intestinal dysbiosis”;

814^  Vladimir Koliadin, “Suppression of non-specific immunity, not T-immunodeficiency, is the main cause of opportunistic infections in AIDS”, April 1998;

815^  Vladimir L. Koliadin, “Destruction of normal resident microflora as the main cause of AIDS”, August 1996;

816^  Peter H. Duesberg, “AIDS acquired by drug consumption and other noncontagious risk factors”, Pharmacology & Therapeutics, 55 (1992) 201-77.

817^  Ross et al., “Conspiracy beliefs about the origin of HIV/AIDS in four racial/ethnic groups”, Journal of Acquired Immune Deficiency Syndrome, 41 (2006) 342-4.

818^  David France, “Challenging the conventional stance on AIDS”, New York Times, 22 December 1998.

819^  For example, Dr. Hershline,

820^  Alan Cantwell, “The secret origins of AIDS: Facts, fallacies & conspiracy theories”, New Dawn Magazine, 9 August 2005;

821^  Juliet Lapidos, “The AIDS Conspiracy Handbook — Jeremiah Wright's paranoia, in context”, Slate, 19 March 2008;

822^  Wangari Maathai, Nobel Peace Prize Laureate: “African Nobel Prize winner says HIV created in lab for biological warfare”,, 12 October 2004;

823^  “Operation INFEKTION: Soviet Bloc intelligence and its AIDS disinformation campaign”;

824^  Alan Cantwell, AIDS And the Doctors of Death: An Inquiry into the Origin of the AIDS Epidemic (Aries Rising Press, 1988); ISBN-10: 0917211251.

825^  Alesha Williams, “Activist tells Long Branch audience of theory on HIV/AIDS virus being man-made — Boyd Graves believes the government targeted blacks”, Asbury Park Press, 21 April 2007;

826^  Angeyo Kalambuka, “Kenya: Don't discount conspiracy theories on origin of Aids”, Daily Nation (Nairobi), 1 December 2009;

827^  Terrell Jermaine Starr, “Blacks targeted? Top AIDS conspiracy theories”, Newsone, 1 December 2011;

828^  Toni Lawson, “Doctors and Nobel Laureate [Wangari Maathai] suggest HIV-AIDS is bio-terrorism”, The Canadian, 15 January 2007;

829^  Chris McGreal, “HIV-infected condoms sent to kill Africans, claims archbishop”, The Guardian, 27 September 2007;,,2177870,00.html

830^  Horowitz & Martin, Emerging Viruses: AIDS and Ebola: Nature, Accident, or Intentional? (Medical Veritas International, 1996); ISBN-10: 0923550127.

831^  Pearce Wright, “Smallpox vaccine ‘triggered Aids virus’”, The Times (London), 11 May 1987.

832^  Edward Hooper, The River : A Journey to the Source of HIV and AIDS (Little Brown, 1999); see also Hooper’s website,

833 ^ |    P. H. Duesberg, “Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation”, Proceedings of the National Academy of Sciences, 86 (1989) 755-64.

834 ^ | | 7.6 | | 8.1 8.3    Henry H. Bauer, Dogmatism in Science and Medicine: How Dominant Theories Monopolize Research and Stifle the Search for Truth (McFarland, 2012)

835^  Henry H. Bauer, “Public Debate about Leung film”,

836^  “DENIED: AIDS denialists disinvited from Congressional hearing — but get indirect endorsement from Rep. Sheila Jackson Lee”, 16 May 2008;

837^  A. Fauci, “Writing for my sister Denise”, AAAS Observer, 1 September 1989, p. 4.

838^  Robert Gallo warned Celia Farber, cited by John Lauritsen, “Truth is bustin’ out all over — HIV symposium at AAAS conference”, New York Native, 18 July 1994;

839 ^ | 7.6 | 7.6.2    J. P. Moore, in the session on “HIV Science and Responsible Journalism”, XVI International AIDS Conference, 13 August 2006.

840 ^ |    “The evidence that HIV causes AIDS”;

841^  Perth Group, “NIH/Antibodies”, (in Internet debate preceding Presidential AIDS Advisory Panel meeting, Johannesburg, July 2000).

842^  Henry H. Bauer, “Answering Cranks — THANK YOU, PERTH!”, 4 December 2009;

843^  Papadopulos-Eleopulos et al., “Evidence-based scientific responses to Jeanne Bergman re House of Numbers”, December 2009;

844^  Papadopulos-Eleopulos et al., “Response to Jeanne Bergman re: ‘House of Numbers’ Lies about Research Findings on T Cells Destruction and AIDS”, November 2009;

845^  Jeanne Bergman, “‘House of Numbers’ lies about research findings on T Cell destruction and AIDS”,

846^  Nathan Geffen, Debunking Delusions: The Inside Story of the Treatment Action Campaign (Jacana Media [Auckland Park, South Africa]), 2010; ISBN 978-1-77009-781-0.

847^  Edwin Cameron with contributions by Nathan Geffen, Witness to AIDS (I. B. Tauris, 2005).

848^  Henry H. Bauer, Review of Debunking Delusions: The Inside Story of the Treatment Action Campaign by Nathan Geffen, Journal of Scientific Exploration, 26 (2012) 677-82.

849^  Henry H. Bauer, Review of Witness to AIDS by Edwin Cameron & Nathan Geffen, Journal of Scientific Exploration, 20 (2006) 436-44.

850 ^ | 7.6.2    Seth C. Kalichman, Denying AIDS: Conspircacy Theories, Pseudoscience, and Human Tragedy (Copernicus/Springer, 2009).

851^  Henry H. Bauer, “Strange case of Dr Jekyll-Kalichman and Mr Hyde-Newton”,

852^  Nicoli Nattrass, The AIDS Conspiracy: Science Fights Back (Columbia University Press, 2012).

853^  Henry H. Bauer, “Nattrass on AIDS”,

854^  Henry H. Bauer, “HIV/AIDS vigilantes protest too much”,

855^  Henry H. Bauer, Review of The AIDS Conspiracy: Science Fights Back by Nicoli Nattrass, Journal of Scientific Exploration, 26 (2012) 793-9.

856^  Henry H. Bauer, “Doctors aren’t scientists, and medicine isn’t science”,

857^  Henry H. Bauer, “Nobel Prizes illustrate that doctors are not scientists”,

858^  Frank Furedi, “Denial: There is a secular inquisition that stigmatises free thinking”, 31 January 2007;

859^  Bernard Barber, “Resistance by scientists to scientific discovery”, Science, 134 (1961) 596-602.

860^  Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson (Cambridge University Press, 1976).

861^  Gunther Stent, “Prematurity and uniqueness in scientific discovery”, Scientific American, December 1972, pp. 84-93.

862 ^   Olen Steinhauer, The Tourist, Minotaur Books, 2009.

863 ^   James Lee Burke, Rain Gods, Simon & Schuster, 2009, p. 177.

864 ^  Henry H. Bauer, "HOW does HIV kill the immune system?",

865 ^   James Lee Burke, Heartwood, Doubleday, 2009, p. 43.

866 ^   Harper et al., "Detection of lymphocytes expressing human T-lymphotropic virus type III in lymph nodes and peripheral blood from infected individuals by in situ hybridization", Proceedings of the National Academy of Sciences USA, 83 (1986) 772-776.

867 ^   Richman et al., "Detecting Human Immunodeficiency Virus RNA in Peripheral Blood Mononuclear Cells by Nucleic Acid Hybridization", Journal of Infectious Diseases, 156 (1987) 823-7.

868 ^   Biberfeld et al., "HTLV-III expression in infected lymph nodes and relevance to pathogenesis of lymphadenopathy", American Journal of Pathology, 125 (1986) 436-42.

869 ^   Numerous reports of heart disease caused by antiretroviral drugs are cited at

870 ^   ”Acquired Immunodeficiency Syndrome (AIDS) — WHO/CDC case definition for AIDS”, Weekly Epidemiological Record, 7 March 1986, 69-73.

871 ^   Callebaut et al., "T-cell activation antigen CD26, as a cofactor for entry of HIV into CD4+ cells", Science, 262 [1993] 2045.

872 ^   Jon Cohen, "HIV 'cofactor' comes in for heavy fire", Science, 262 [1993] 1971.

873 ^   Jon Cohen, “Likely HIV cofactor found", Science, 272 [1996] 809-10.

874 ^ |    Celia Farber, "Positively Flawed: Welcome to the Machine", Impression, June 1999;

875 ^ 3.3.1 | | 4.7.6    UNAIDS, 2008 Report on the Global AIDS Epidemic.

876 ^   J. C., "Thailand points the way", Science, 270 (1995) 30.

877 ^   National Institute of Allergy and Infectious Diseases, "Trojan Horse Virus controls HIV infection", 4 September 1997.

878 ^   Tom Nurre, "Radical research", Angelo State University Magazine, Summer 2011, 16-9.

879 ^   Buckley et al., "HIV protease-mediated activation of sterically capped proteasome inhibitors and substrates", Journal of the American Chemical Society, 133 (2011) 698-700.

880 ^   Orli Van Mourik, "Good vibrations vs. bad viruses", Discover, June 2008, p. 16.

881 ^   Cavrois, Neidleman & Greene, "The Achilles Heel of the Trojan Horse Model of HIV-1 trans-infection" PLoS Pathogen, 4(#6, 2008): e1000051.

882 ^   refs 34, 120-5, 131-2 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232.

883 ^   refs. 35-43, 103 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232.

884 ^   Refs 74, 76, 77, 84, 89, 93-100, 102 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232.

885 ^   Refs. 35, 38, 39, 41, 104-6, 111-6 in Pinzone et al., Vitamin D deficiency in HIV infection: an underestimated and undertreated epidemic, European Review for Medical and Pharmacological Sciences, 17 (2013) 1218-1232.

886 ^   Rick Weiss, "Doctor hopes to repeat baboon cell transplant", Washington Post, 11 February 1996, p. A9.

887 ^   Lawrence K. Altman, "The Doctor's World; Baboon cells might repair AIDS-ravaged immune systems", New York Times, 19 July 1994.

888 ^   "42-yr-old Glen Elder, dead of heart attack at 42", Chronicle of Higher Education, 12 June 2009, A33.

889 ^ | 6.4.2    "Jeff Getty, 49, AIDS activist who received baboon cells, is dead", New York Times, 16 October 2006.

890 ^   Jonathan Kellerman, Devil's Waltz, Bantam 1993, p. 336.

891 ^   Colin Thubron, "Believers' bazaar", review of In Search of the Sacred in Modern India by William Dalrymple, New York Times Book Review, 18 July 2010, p. 19.

892 ^   Gurav & Blanchard, "Disease, Death and Dhandha: Gharwali's Perspectives on the Impact of AIDS on Devadasi System and the Sex Work in South India", World Journal of AIDS, 3 (2013) 26-32.

893 ^   Henry H. Bauer, "HIV" is NOT sexually transmitted — yet more clear evidence,

894 ^   Edmund White, States of Desire, Plume/Penguin, 1991.

895 ^   Edmund White, City Boy: My Life in New York During the 1960s and '70s, Bloomsbury, 2009.

896 ^   James, commenter, Henry H. Bauer, Reminiscing; not much new under the sun; why gay men and Africans are the predominant victims.

897 ^ |    David Crowe, "Predictability of a CD4 Count", July 2012.

898 ^   Henry H. Bauer, The LAZARUS EFFECT in HIV/AIDS, May 10, 2010.

899 ^   Henry H. Bauer, The Lazarus Effect and the puzzle of delayed illness in "HIV-positive" gay men, May 6, 2014.

900 ^   Amanda Bennett & Anita Sharpe, "AIDS fight is skewed by federal campaign exaggerating risks", Wall Street Journal, 1 May 1996, A1, 6.


902 ^   Viral/Molecular Core Virology Services: Prototype HIV-1 Strains.

903 ^   Viral/Molecular Core Virology Services: Primary HIV-1 Isolates.

904 ^   Viral/Molecular Core Virology Services: HIV-1 Mutant Viruses.

905 ^   Goodenow et al., "HIV-1 isolates are rapidly evolving quasispecies: evidence for viral mixtures and preferred nucleotide substitutions", Journal of Acquired Immune Deficiency Syndromes, 2 (1989) 344-52.

906 ^   Lukashov et al., "The genetic diversity of HIV-1 and its implications for vaccine development", chapter 3 (pp. 93-120) in AIDS Vaccine Rresearch, ed. Wong-Staal & Gallo, Marcel Dekker, 2002.

907 ^   "Does HIV cause AIDS? Denialism vs. pro ARVs (DEBATE)", mariatmejia, 19 January 2011.

908 ^   Henry H. Bauer, "AIDS and Idiopathic CD4-T-cell Lymphopenia".

909 ^   Zonios et al., "Idiopathic CD4 lymphocytopenia: a case of missing, wandering or ineffective T cells", Arthritis Research & Therapy, 14 (2012) 222.

910 ^   W. A. Blattner, "Retroviruses", pp. 545-592 in Viral Infections of Humans, ed. A. S. Evans, Plenum Medical Book Company (3rd ed., 1989).

911 ^   Patricia Goodson, "Questioning the HIV-AIDS hypothesis: 30 years of dissent", Frontiers in Public Health, 2 [Article 154] (2014) 1-11.

912 ^   David Crowe, "Needle Exchange Programs (NEP) and HIV", Conquering Addictions Together Coquitlam, BC, March 28-29, 2014.

913 ^ |    M. Aziz, "Commentary on summary of Penrose Inquiry report", Immunity Resource Foundation, March 26, 2015.

914 ^   Donald W. Miller, Jr., "HIV/AIDS: Unmasking Falsehood, Bringing Truth to Light",, August 7, 2015.

915 ^   B. Lau, S. J. Gange & R. D. Moore, Journal of Acquired Immune Deficiency Syndromes, 44 (2007) 179-87.

916 ^   Laurence Brunet, Erica E. M. Moodie, Jim Young, Joseph Cox, Mark Hull, Curtis Cooper, Sharon Walmsley, Valérie Martel-Laferrière, Anita Rachlis & Marina B. Klein for the Canadian Co-infection Cohort study, "Progression of liver fibrosis and modern combination antiretroviral therapy regimens in HIV-hepatitis C co-infected persons", Clinical Infectious Diseases, published online 23 September 2015; doi:10.1093/cid/civ838.

917 ^   Pakker et al., "Immune restoration does not invariably occur following long-term HIV-1 suppression during antiretroviral therapy. INCAS Study Group", AIDS, 13 (1999) 203-12.

918 ^ 3.3.3 |    CDC, HIV Transmission Risk, last reviewed 16 November 2015.

919 ^    Masson et al., "Genital inflammation and the risk of HIV acquisition in women", Clinical Infectious Diseases, 61 (2015):260-9.

920 ^    Katharine Child, "SA's women most at risk of getting HIV", TimesLive, 29 June, 2015.

921 ^   Cowell et al., "Trends in hospital deaths Among Human Immunodeficiency Virus–infected patients during the Antiretroviral Therapy era, 1995 to 2011", Journal of Hospital Medicine, 10 (2015) 608-14.

922 ^   Nishana et al., "HIV integrase inhibitor, Elvitegravir, impairs RAG functions and inhibits V(D)J recombination", Cell Death and Disease, 8 (2017):e2852. doi: 10.1038/cddis.2017.237; open access, 14 pp.

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