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HIV does not cause AIDS

Henry Bauer
Source: Edge Science
May-June 2010 issue

“What everyone knows” is sometimes wrong. When it comes to science, including medical science, history might even suggest that what everyone knows at any given time turns out later to have been wrong to some degree: scientific understanding has progressed, after all, and it has often progressed by overturning earlier theories.

But even as it's widely recognized that science has progressed, it's usually forgotten that this very progress has often meant superseding or rejecting earlier ideas. And the notion that a contemporary consensus might be wrong seems unbelievable to most people.

So the claim that HIV doesn't cause AIDS, when everyone knows that it does, is treated by the media, the public, and mainstream science as not worth attending to. And yet the proof that HIV cannot be the cause of AIDS is at hand in the technical literature, as well as in dozens of books aimed mainly at a general audience.

To consider that proof, it's necessary not only to specify that evidence but also to provide some assurance that good alternative explanations are available for what AIDS is and what HIV is. So those questions will be answered after outlining the reasons why the HIV=AIDS theory is wrong.

The Evidence that HIV Doesn't Cause AIDS[1]

  1. If HIV is the cause of AIDS, then there ought to be an obvious correlation between the presence of HIV and the incidence of AIDS. There isn't. HIV and AIDS are not correlated chronologically; they have changed differently over time. Nor are they correlated geographically: even from the very beginning, places of high HIV were not places of high AIDS. Furthermore, the relative impact on men and women is quite different—the male-to-female ratio for HIV has hardly changed over the years, while the ratio for AIDS has changed dramatically. So too with white and black Americans—the black-to-white ratio for HIV has hardly changed over the years, while the ratio for AIDS has changed dramatically (chapter 9 in 1).

    If HIV causes AIDS, why then are there HIV-negative AIDS cases? Just how many is not known because after a substantial number had been reported, they were explained away as cases of a new disease, “idiopathic CD4 T-cell lymphopenia”—meaning deficiency of CD4 cells for no known reason, which is precisely the same definition as that of AIDS before the claimed discovery of HIV as cause of the immune deficiency (pp. 19–20 in 1).

    There are also HIV-positive people who have remained AIDS-free for more than 20 years, the so-called “long-term non-progressors” or “elite con trollers” (p. 95 in 1). The mainstream acknowledges this, but treats it as a mystery to be solved: why do some people have an uncanny ability to stave off either infection or, if infected, to stave off the harmful action of HIV? The mainstream view is that this is a rarity. However, since not every healthy person has been tested for HIV, it cannot be known with any certainty how many long-term non-progressors there actually are. Available data suggest that in the United States it might be as many as half of all people who would test HIV-positive.2

  2. The lack of correlation between HIV and AIDS numbers ought to be enough to settle the matter. But with so long and firmly entrenched a belief, there is no question of overkill by enumerating further strikes against HIV/AIDS theory. So it is worth noting that, whatever HIV may be, it is not something infectious:

    • The estimated number of HIV-positive Americans has hovered around 1 million from the earliest time, the mid-1980s, to the present (pp. 1–2 in 1), whereas the incidence of infections increases and decreases.

    • In any given group, the tendency to test HIV-positive varies with age, sex, and race in the same manner. Infectious diseases do not display those regular trends (sources cited throughout Part I of 1). Infection is asserted to occur via blood, including transmission via dirty needles, and via mothers' milk, but chiefly through sexual activity. However:

    • There are no authenticated cases of AIDS from accidental health-care-worker needle-sticks (p. 48 in 1).

    • More breastfeeding correlates with less, not more, incidence of “HIV-positive” among the babies.3

      Sexual transmission of HIV has never been proven. The largest prospective study, in which discordant couples (one partner HIV-positive, the other negative) were followed over a period of years, could report no instances where the negative partner became positive.4

    • Incidence of HIV does not parallel that of known sexually transmitted infections (STIs); often rates of HIV went up as those of such STIs as gonorrhea or syphilis decreased, and vice versa. (p. 31 ff. and passim in 1)

    • Use of condoms doesn't decrease the incidence of HIV-positive (sources cited in 5 and p. 44 in 1).

    • A literally impossible level of sexual promiscuity is required to explain the prevalence of “HIV” in Africa—20–40% of adults having multiple sexual partners and changing them frequently.6

    • Pregnant women become HIV-positive more often than do non-pregnant women.7

  3. According to HIV/AIDS theory, the “viral load” determined by polymerase chain reaction (PCR) represents the amount of HIV present, which determines how rapidly the relevant immune-system-cells (CD4 T-cells) are killed off and therefore predicts the course of illness toward eventual death. However, there is no correlation between viral load and CD4 counts.8 The official Treatment Guidelines9 speaks of three separate types of treatment failure: virologic, immunologic, and poor patient prognosis. If the theory were correct, then failure of one would bespeak failure of the others.

  4. More than two decades of attempts to vaccinate against becoming HIV-positive have all failed. No satisfactory explanation for such failure has been offered, nor have the successive failures turned up clues to possible success.

  5. More than two decades of attempts have failed to develop any microbicide that could inactivate HIV to prevent incidence of HIV-positive. Again, no satisfactory explanation for such failure has been offered. Microbicides containing anti-retroviral drugs, which purportedly kill HIV in vivo, have not been effective as preventive microbicides.

  6. HIV/AIDS theory asserts that there is an average latent period of about 10 years between infection by HIV and signs of actual illness. The actual data reveal no sign of such a latent period. The median age at which people first test HIV-positive, the median age of people “living with AIDS” or “living with HIV,” and the median age of people who die from “HIV disease” are all roughly the same: namely, the prime years of adulthood, 35–50.10



What is AIDS?

A huge complication is that the official definition of AIDS has been changed, moreover quite drastically, several times. The original, early-1980s, pre-HIV-discovery AIDS is not the same as present-day AIDS. A particularly portentous change in definition came in 1993.

It was around 1980 that, it's commonly said, doctors first noted that “young, previously healthy, gay men” were presenting with diseases formerly associated with immune suppression in transplant patients or in old people or babies with insufficiently competent immune systems. Given the concentration among gay men, the phenomenon was described as Gay Related Immune Deficiency (GRID). The predominant manifest illnesses were Kaposi's sarcoma (KS), purple blotches on skin and elsewhere; Pneumocystis carinii pneumonia (PCP); and candidiasis (thrush, yeast infections).

GRID was soon re-named AIDS—Acquired Immune Deficiency Syndrome—to avoid placing the stigma for the disease solely on gay men. A considerable body of evidence suggested that KS resulted from excessive exposure to nitrites, known as “poppers,” which were in ubiquitous use in gay circles. A heavy strike against HIV/AIDS theory is that since the early 1990s KS has been attributed to a herpes virus (HHV-8 or KSHV), not to HIV, because there were many HIV-negative KS patients, many of whom had normal or even high immune-system cell-counts.

Initially, PCP had been thought to be a bacterial or parasitic infection, but it was later recognized that it is actually fungal, as is candidiasis. A plausible explanation for the rather sudden increase in those fungal infections among gay men, about a decade after Gay Liberation, indicts certain practices that can damage the intestinal microfora (beneficial bacteria) that protect against fungal infections in particular. Those practices include intensive rectal douching and excessive resort to antibiotics, sometimes for treatment of recurrent infections (gonorrhea, syphilis, herpes, and more) but sometimes even for prophylaxis.11

For descriptions of the unhealthy “fast-lane” lifestyle pursued by a small proportion of gay men, see for example Larry Kramer's novel Faggots12 and the documentary film When Ocean Meets Sky.13

Moreover, it turns out that the first AIDS cases were not “young, previously healthy, gay men.” Their average age was in the late 30s, they were anything but previously healthy, and their salient common characteristic was not that of being gay.

It was their excessive use of recreational drugs (p. 186 ff. in 1), average age, and medical history that made a lifestyle explanation of AIDS highly plausible. The lifestyle explanation had not been universally accepted, however, in particular not by virologists, who were at something of a loose end after a decade or two of unsuccessfully looking for human-cancer-causing viruses.14

HIV became acknowledged as the cause of AIDS following a press conference called by the Secretary for Health and Human Services, before any scientific publication on the matter, and the subsequent publications came nowhere near establishing the claim. For example, HIV was only found in two-thirds of all AIDS cases, and the patented test for HIV, which actually is for antibodies against HIV, turned out to give positive results even in many cases when the virus itself could not be detected by actual culture (for details and pertinent sources, see pp. 196–7 in 1).

Still, the imprimatur of the Secretary for Health and Human Services and the attraction of grants from the National Institutes of Health, a subsidiary of the Department of Health and Human Services, brought virologists almost universally to research on HIV, and the Centers for Disease Control and Prevention (CDC) soon accepted the theory that HIV was the cause of AIDS. Thereafter, CDC progressively increased the number of illnesses that it regards as “AIDS-defining,” just because some significant number of the patients tests HIV-positive, in tuberculosis, for example, or with cervical cancer.

Those diseases are neither new nor opportunistically dependent on finding already damaged immune systems to attack, and so “AIDS” nowadays is an entirely different matter than the original GRID that was later re-named AIDS.

AIDS was originally a lifestyle phenomenon associated with particular damage to the intestinal flora. AIDS nowadays is any disease where an appreciable number of patients test HIV-positive.

What is HIV?

Possibly the most incredible part of this story is the demonstrable fact that HIV tests do not detect HIV. An incredible part of that incredible story is that HIV has never been isolated in pure form, leaving ample room for the claim that HIV has never been proven to exist.15

A recent article16 reviews the relevant points:

  • The original HIV test was based on selecting proteins that reacted strongly with something in the sera from AIDS patients, presumed to be antibodies to a presumed AIDS-causing virus.

  • However, that these are HIV antibodies could only be confirmed with authentic virus, and no pure samples of virus have ever been prepared by isolation direct from an AIDS patient or after culturing.

  • All later tests have been “validated” by demonstrating that they test positive when the original (Abbott Laboratories) test does. There is no “gold standard” for HIV tests and cannot be, since no pure virus has ever been prepared. The so-called confirmatory tests, typically the Western Blot but including the putative “viral load” measurements, are not confirmatory. As Weiss & Cowan17 point out, they should be called “supplemental,” not confirmatory.

  • Rodney Richards18 has described how “antibody positive” came to be taken as proof of active infection, without the benefit of evidence to that effect.

  • An authoritative description 17 for detecting actual HIV infection makes plain that the tests in themselves are insufficient. In a population known to be at low risk—i.e., where the incidence of AIDS and presumably HIV is low (HIV ~ 0.1%)—a positive “HIV” test may be a false positive 5 out of 6 times if the test has a nominal specificity and sensitivity of 99.5%.

  • In practice, the tests were calibrated to have high sensitivity, and therefore reduced specificity, because they were intended for and were approved only for screening blood supplies, where sensitivity matters a great deal but false positives mean only the discarding of some blood.

  • When the tests are misused, as they currently are, to bespeak actual infection, considerable harm ensues to individuals who are told they are HIV-positive, and the psychological harm is compounded with physical harm if they receive antiretroviral drugs. Those drugs, widely called “life-saving,” are seriously toxic; the Treatment Guidelines19 have acknowledged for some years that patients receiving antiretroviral treatment experience fewer AIDS events than such serious adverse non-AIDS events as organ failure (of heart, kidney, or liver) and cancer that are typical consequences of toxic medication.



So what is HIV?

It is a postulated but never isolated retrovirus. In practice, HIV means whatever is detected by an HIV test. But those tests are known to generate a high rate of false positives, especially in populations not evidently at risk; you can test HIV-positive after a fu vaccination, for example, and for dozens of other reasons.20

In any case, since rates of positive HIV tests do not correlate with incidence of AIDS, the question of what HIV tests really detect is moot as far as AIDS is concerned.

In Conclusion

The belief that HIV causes AIDS gained hold and then hegemony as a result of hasty actions based more on political than scientific considerations, and the unwarranted consensus has had tragic consequences.21

The conventional wisdom was taught that HIV inevitably leads to AIDS, that it is highly infectious, and that it is so life-threatening that even treatment with highly toxic medications represents a good compromise, even when it involves iatrogenic damage to pregnant women, the unborn, and the newly born. A perusal of the “side” effects of all the antiretroviral drugs, set out in the official Treatment Guidelines, makes the toxicity of these chemicals painfully obvious. AZT—nowadays usually called ZDV, zidovudine, brand name Retrovir—has been in use for more than two decades, virtually exclusively for the first decade. As its side effects the Treatment Guidelines (Table 12, 1 December 2009) list bone marrow suppression (“Onset: Few weeks to months”); gastrointestinal intolerance (immediate); liver damage (over months or years); disturbance of lipid metabolism (within weeks to months) with risk of diabetes; severe mitochondrial damage and lactic acidosis (within months); and Stevens-Johnson syndrome, or toxic epidermal necrosis (days to weeks). AZT was recently listed as a carcinogen in the State of California. Nevertheless, it still forms part of the “preferred” treatment regimen for pregnant women (Table 5a in the Treatment Guidelines).

The mistaken belief that HIV causes AIDS has damaged the health of untold numbers of people around the world.

Henry Bauer is Professor Emeritus of Chemistry & Science Studies and Dean Emeritus of Arts & Sciences at Virginia Tech. Bauer has served as the editor of the Journal of Scientific Exploration. His latest book is The Origin, Persistence and Failings of HIV/AIDS Theory.



notes

  1. Henry H. Bauer, The Origin, Persistence and Failings of HIV/AIDS Theory, McFarland (2007).
  2. Matteo P. Galletti and Henry H. Bauer, “Safety issues in didactic anatomical dissection in regions of high HIV prevalence,” Italian Journal of Anatomy and Embryology, in press.
  3. Scientifc publications cited in Henry H. Bauer, “More HIV, less infection: The breastfeeding conundrum,” 21 November 2007, http://wp.me/p8Qhq-e; “HIV and breastfeeding again,” 13 February 2008, http://wp.me/p8Qhq-1t
  4. N. S. Padian, S. C. Shiboski, S. O. Glass, and E. Vitting-hoff, “Heterosexual transmission of human im munodefciency virus (HIV) in Northern California: results from a ten-year study,” American Journal of Epidemiology, 146 (1997) 350-7.
  5. Scientifc publications cited in Henry H. Bauer, “HIV and sexually transmitted disease: It just isn’t so,” 28 November 2007, http://wp.me/p8Qhq-i; “Condoms and HIV: What everyone knows is once again wrong,” 10 February 2008, http://wp.me/p8Qhq-1r; “Circumcision and condom idiocies,” 10 November 2009, http://wp.me/p8Qhq-gD
  6. James Chin, The AIDS Pandemic: The Collision of Epidemiology with Political Correctness, Radcliffe Publishing, 2007.
  7. Sources cited in Henry H. Bauer, “Why pregnant women tend to test ‘HIV-positive’,” 5 October 2009, http://wp.me/p8Qhq-hC; “Spontaneous generation of ‘HIV’,” 25 October 2009, http://wp.me/p8Qhq-hE.
  8. Benigno Rodríguez, Ajay K. Sethi, Vinay K. Cheruvu, Wilma Mackay, Ronald J. Bosch, Mari Kitahata, Stephen L. Boswell, W. Christopher Mathews, David R. Bangsberg, Jeffrey Martin, Christopher C. Whalen, Scott Sieg, Suhrida Yadavalli, Steven G. Deeks, and Michael M. Lederman, “Predictive value of plasma HIV RNA level on rate of CD4 T-Cell decline in untreated HIV infection,” JAMA, 296 (2006) 1498–1506.
  9. Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health and Human Services; http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf.
  10. Henry H. Bauer, “Incongruous age distributions of HIV infections and deaths from HIV disease: Where is the latent period between HIV infection and AIDS?” Journal of American Physicians & Surgeons, 13 (#3, Fall 2008) 77–81.
  11. Tony Lance, “Gay-related Intestinal Dysbiosis”; http://hivskeptic.fles.wordpress.com/2008/02/gay-relatedin-testinaldysbiosis.pdf.
  12. Larry Kramer, Faggots, Random House, 1978.
  13. When Ocean Meets Sky; flm by Crayton Robey, 2006; shown periodically on the LOGO television channel; http://www.whenoceanmeetssky.com.
  14. Peter Duesberg, Inventing the AIDS Virus, Regnery, 1996, chapter 4.
  15. The Perth Group; http://www.theperthgroup.com.
  16. Henry H. Bauer, “HIV Tests are not HIV Tests,” Journal of the American Physicians and Surgeons, vol. 15, 2010, pp. 5–9.
  17. Stanley H. Weiss and Elliott P. Cowan, “Laboratory detection of human retroviral infection,” Chapter 8 in AIDS and Other Manifestations of HIV Infection, ed. Gary P. Wormser, 4th ed. (2004).
  18. Rodney Richards, “The birth of antibodies equals infection,” App. II, pp. 333–40 in Celia Farber, Serious Adverse Events: An Uncensored History of AIDS, Melville House, 2006.
  19. Reference ix: p. 21 in 3 November 2008 version, p. 13 in 29 January 2008 and 1 December 2007 versions.
  20. Christine Johnson, “Whose antibodies are they anyway? Factors known to cause false positive HIV antibody test results,” Continuum 4 #3, Sept./Oct. 1996; http://www.virusmyth.net/aids/data/cjtestfp.htm.
  21. Robert Root-Bernstein, Rethinking AIDS: The Tragic Cost of Premature Consensus, Free Press, 1993.


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