H.I.V. is a harmless passenger virus that DOES NOT cause AIDS. National Academy of Sciences member Peter Duesberg has been preaching flaws in the HIV causing AIDS hypothesis since 1987. One supporter of this conclusion is Kary Mullis, Nobel Prize winner in Chemistry and inventor of PCR, who wrote an introduction to Duesberg's book Inventing the AIDS Virus (1997). Other supporters include several other whistle blowers , not to mention the dozens of doctors, professors, and medical researchers who are part of the The Group for the Scientific Reappraisal of the HIV-AIDS Hypothesis since 1991. The fraud of the HIV-AIDS hypothesis seems to be becoming more and more public, considering at least 15 books by a dozen different authors have been published on this almost taboo topic. Filmmaker Robin Scovill created the documentary The Other Side of AIDS which won a Special Jury Prize at the 2004 AFI Los Angeles International Film Festival. Serge Lang was a dissident and a professor emeritus of mathematics at Yale University. One of the newer dissidents is Rebecca Culshaw, who wrote her PhD dissertation on math models of HIV infection.
Over the last four years, I have read: Duesberg's Inventing the AIDS Virus (1997), Harvey Bialy's Oncogenes, Aneupolidy, and AIDS (2004) , and most of Duesberg's scientific papers on his website. Bialy was the scientific editor of the Nature Biotechnology journal from 1984 to 1996. Duesberg's incredibly dense 1987 Cancer Research journal article that shows his early logic -as well as the depth of his knowledge as one of the world's most knowledgeable researchers -convinced me to read Duesberg's book; the fulltext of the 20+ page review article with 278 citations can be read in HTML format on Duesberg's website, but I recommend reading it in its original journal format by downloading the .pdf (5637 K in size) from the journal's website. The best summary for laymen that I have come across is a 20-page article by science fiction writer James P. Hogan. To get a quick idea of the vehement level of dissent in the scientific community, read this 1-page letter (.pdf file) from several researchers that was published in Nature in 2000. Duesberg's most recent scientific paper (.pdf file) "The Chemical Bases of the Various AIDS Epidemics: Recreational Drugs, Anti-viral Chemotherapy and Malnutrition" was published in 2003 in Journal of Biosciences.
For reference, a mainstream chronology of the progression of the AIDS "virus" can be found here .
James P. Hogan explains in the following excerpts from his essay how the relatively rare disease of AIDS has been publicly exaggerated into an "epidemic":
(from page 5 and 6)
For example, statistics for new AIDS cases were always quoted as cumulative figures that could only get bigger, contrasting with the normal practice with other diseases of reporting annual figures, where any decline is clear at a glance. And despite the media's ongoing stridency about an epidemic out of control, the actual figures from the Centers for Disease Control (CDC), for every category, were declining, and had been since a peak around 1988. This was masked by repeated redefinitions to cover more diseases, so that what wasn't AIDS one day became AIDS the next, causing more cases to be diagnosed. This happened five times from 1982 to 1993, with the result that the first nine months of 1993 showed as an overall rise of 5% what would otherwise--i.e. by the 1992 definition--have been a 33% drop.5
Currently (January, 2003) the number indicator diseases is 29. One of the newer categories added in 1993 was cervical cancer. (Militant femininists had been protesting that men received too much of the relief appropriations for AIDS victims.) Nobody was catching anything new, but suddenly in one group of the population what hadn't been AIDS one day became AIDS the next, and we had the headlines loudly proclaiming that heterosexual women were the fastest-growing AIDS group.
A similar deception is practiced with percentages, as illustrated by figures publicized in Canada, whose population is around 40 million. In 1995, a total of 1410 adult AIDS cases were reported, 1295 (91.8%) males and 115 (8.2%) females. 1996 showed a startling decrease in new cases to 792, consisting of 707 males (89.2%) and 85 females (10.8%). So the number of adult female AIDS cases actually decreased by 26% from 1995 to 1996. Yet, even though the actual number decreased, because the percentage of the total represented by women increased from 8.2% in 1995 to 10.8% in 1996, the Quarterly Surveillance Report (August 1997) from the Bureau of HIV/AIDS and STD at the Canadian Laboratory Centre for Disease Control issued the ominous warning that AIDS cases among Canadian women had dramatically increased.6
Meanwhile, a concerted campaign across the schools and campuses was doing its part to terrorize young people over the ravages of teenage AIDS. Again, actual figures tell a different story. The number of cases in New York City reported by the CDC for ages 13-19 from 1981 to the end of June 1992 were 872. When homosexuals, intravenous drug users, and hemophiliacs are eliminated, the number left not involving these risks (or not admitting to them) reduces to a grand total of 16 in an 11 year period. (Yes, sixteen. You did read that right.)75 Root-Bernstein, 1993
6 Maggiore, 2000, p.46
7 Thomas, 1993
(from page 11)
In a mass screening in Russia in 1991, the WHO performed 30 million tests over a two-year period and found 30,000 positive results. Attempts to confirm these yielded around 300, of which 66 were actual AIDS cases.16
16 Shenton, 1998, p.164
So, with no scientific evidence, why in April 1984 did Margaret Heckler, the U.S. Secretary of Health and Human Services, announce to the world that HIV caused AIDS ?
Reading the wikipedia article on Heckler ,
- 1) Heckler's professional background is in law not medicine ,
- 2) her previous occupation was as a Congressman in a state (Massachusetts) with perhaps the most powerful medical and biotech industry lobbies of all states,
- 3) also in 1984 (same year as the HIV causing AIDS announcement), her husband John filed for divorce: "Heckler publicly criticized his wife for becoming a changed person after she entered politics, and cited “fear of life and limb and mental welfare” in his filing "
In 1983, Dr. Brandt said that investigating the disease had become “the No. 1 priority” of the Public Health Service. At the time, only 1,450 AIDS cases had been reported.Brandt had a phD in math along with a medical degree, so he was no dummy. Was he the brains, and Heckler the willing (or threatened) public servant of the medical/biotech lobbies?
Dr. Brandt was also instrumental in finding a way for the disease control centers to build a maximum security laboratory, which the agency needed to investigate a growing number of dangerous microbes, but which the Reagan administration had blocked, Dr. Foege said.
In addition to his medical degree, Dr. Brandt had a Ph.D. in mathematics, and he used that training in his various jobs, so it was not easy to fool him with numbers, Dr. Foege said. Yet Dr. Brandt drew widespread criticism for making an overly optimistic prediction for when an AIDS vaccine would be available.
At a news conference in 1984, Dr. Brandt’s boss, Health and Human Services Secretary Margaret M. Heckler, announced that scientists at the National Institutes of Health in Bethesda, Md., had discovered the AIDS virus. But she gave little credit to Dr. Luc Montagnier’s team from the Pasteur Institute in Paris, which had also discovered the virus.
Ms. Heckler also said that an AIDS vaccine would be tested in two years and Dr. Brandt said he was optimistic that a marketable one would be available in three years, or 1987.
When reporters said that Dr. Montagnier had told them it would take 5 to 10 years, Dr. Brandt stood by his three-year prediction.
Now experts say that making an AIDS vaccine is far more complex than originally believed. Any vaccine is years away from being licensed and might protect a much smaller proportion of recipients than other standard immunizations.
The HIV/AIDS dogma is one of the dominating myths of our time, so I am reluctant to believe that the announcement did not have official support from more than just some former Massachusetts congressman and a super-smart Texas doctor. I am assuming that the announcement was made with the approval of the highest levels of government, considering AIDS federal funding and private donations (like from the Bill and Melinda Gates Foundation) seem to keep increasing.
So,what might the possible reasons be for propagating the myth?
- military concerns about needing more research in case of biological warfare ?
- Naval War College professor and grand strategist Thomas P.M. Barnett mentioned in a radio interview that the main concern after nuclear weapons in the wrong hands is biological weapons
- promoting a mood of conservatism to counter the societal chaos of the 1960s and 1970s
- possible covert funding for off-the-record foreign aid or projects ???
- the odd thing about third-world nations who artificially inflate their number of AIDS cases for the purpose of obtaining foreign aid/donations is that the lies will absolutely destroy these nations' tourism, as well as probably decrease F.D.I. in the long-term
- Of course, the numbers produced by mainstream organizations from W.H.O. or the U.N. could theoretically counter - in whatever desired direction, drastically up or drastically down - the numbers of some trouble-making nations for political purposes
- population control across the globe (first, second, and third world)
- an attempt to slow-down the rapid population growth in the third-world, since slower growth means more stability, by encouraging birth control
- however, long-term declines in the growth rate are statistically most likely after industrialization and widespread higher education attainment
- medical/biotech industries
- reaping huge profits from publicly funded and paid for drugs, even the drugs that don't work or are poison
- covering up the failures of the "War on Cancer" with another distraction - HIV/AIDS - that the public will be fearful not to continue throwing public money to bloated medical institutions that would continue to get even more bloated
- to forestall opposition to drastic cuts to Medicare or Medicaid - which have greatly inflated medical costs in the U.S. since they were created - during a climate of the public wanting budget cuts
- financial institutions (Wall Street) reaping huge commissions for issuing I.P.O.s to biotech companies that have NO BUSINESS PLAN (like many of the dot-com busts)
EXCERPT FROM James P. Hogan's article "AIDS Heresy In The Viricentric Universe" (pages 8-12)
SCIENCE BY PRESS CONFERENCEEXCERPT FROM Rebbecca Culshaw's article "Why I Quit HIV" :
So how did HIV come to be singled out as the cause to begin with? The answer seems to be, at a press conference. In April, 1984, the Secretary of Health and Human Services, Margaret Heckler, sponsored a huge event and introduced the NIH researcher Robert Gallo to the press corps as the discoverer of the (then called HTLV-III) virus, which was declared to be the probable cause of AIDS. This came before publication of any papers in the scientific journals, violating the normal protocol of giving other scientists an opportunity to review such findings before they were made public. No doubt coincidentally, the American claim to fame came just in time to preempt the French researcher Luc Montagnier of the Pasteur Institute in Paris, who had already published in the literature his discovery of what later turned out to be the same virus.
From that point on, official policy was set in stone. All investigation of alternatives was dropped, and federal funding went only to research that reflected the approved line. This did not make for an atmosphere of dissent among career- minded scientists, who, had they been politically free to do so, might have pointed out that even if the cause of AIDS were indeed a virus, the hypothesis of its being HIV raised some distinctly problematical questions.
Proponents of the HIV dogma assert repeatedly that "the evidence for HIV is overwhelming." When they are asked to produce it or cite some reference, the usual response is ridicule or some ad hominem attack imputing motives. But never a simple statement of facts. Nobody, to my knowledge, has ever provided a definitive answer to the simple question, "Where is the study that proves HIV causes AIDS?" It's just something that "everybody knows" is true. Yet despite the tens of thousands of papers written, nobody can produce one that says why. Reference is sometimes made to several papers that Gallo published in Science after the press conference, deemed to have settled the issue before any outside scientists had seen them.11 But even if the methods described are accepted as demonstrating true viral isolation as claimed, which as we've seen has been strongly disputed, they show a presence of HIV in less than half of the patients with opportunistic infections, and less than a third with Kaposi's sarcoma--the two most characteristic AIDS diseases. This is "overwhelming" evidence? It falls short of the standards that would normally be expected of a term-end dissertation, never mind mobilizing the federal resources of the United States and shutting down all investigation of alternatives. And the case gets even shakier than that.
Biology's Answer to Dark Matter? The Virus that Isn't There
Viruses make you sick by killing cells. When viruses are actively replicating at a rate sufficient to cause disease, either because immunity hasn't developed yet or because the immune system is too defective to contain them, there's no difficulty in isolating them from the affected tissues. With influenza, a third of the lung cells are infected; with hepatitis, just about all of the liver cells. In the case of AIDS, typically 1 in 1000 T-cells shows any sign of HIV, even for terminally ill cases--and even then, no distinction is made of inactive or defective viruses, or totally non- functional viral fragments. But even if every one were a lethally infected cell, the body's replacement rate is 30 times higher. This simply doesn't add up to damage on a scale capable of causing disease.12
Most people carry traces of just about every microbe found in their normal habitat around with them all the time. The reason they're not sick all the time is that their immune system keeps the microbes inactive or down to numbers that can't cause damage.
According to Dr. Etienne de Harven, emeritus Professor of Pathology, University of Toronto, who worked on the electron microscopy of retroviral structures for 25 years at the Sloan Kettering Institute in New York, "Neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus in AIDS patients."13
11 Science 224: 497-500; 503-505; 506-508 (1984)
12 Duesberg, 1992, p.210
13 De Harven, 1998
Retroviruses, the class to which HIV belongs, survive by encoding their RNA sequences into the chromosomal DNA of the host cell (the reverse of the normal direction of inform ation flow in cell replication, which is DNA to RNA to protein, hence the name). When that part of the host chromosome comes to be transcribed, the cell's protein- manufacturing machinery makes a new retrovirus, which leaves by budding off through the cell membrane. The retrovirus, therefore, leaves the cell intact and functioning, and survives by slipping a copy of itself from time to time into the cell's normal production run. This strategy is completely different from that of the more prevalent "lytic" viruses, which take over the cell machinery totally to mass-produce themselves until the cell is exhausted, at which point they rupture the membrane, killing the cell, and move on, much in the style of locusts. This is what gives the immune system problems, and in the process causes colds, flu, polio, rabies, measles, mumps, yellow feve r, and so on.
But a retrovirus produces so few copies of itself that it's easy meat for an immune system battle-trained at dealing with lytic viruses. For this reason, the main mode of transmission for a retrovirus is from mother to child, meaning that the host organism needs to live to reproductive maturity.14 A retrovirus that killed its host wouldn't be reproductively viable. Many human retroviruses have been studied, and all are harmless. (Some rare animal cancers arise from specific genes inserted retrovirally into the host DNA. But in these cases tumors form rapidly and predictably soon after infection--completely unlike the situation with AIDS. And a cancer is due to cells proliferating wildly--just the opposite of killing them.)
HIV conforms to the retroviral pattern and is genetically unremarkable. It doesn't kill T-cells, even in cultures raised away from a body ("in vitro"), with no immune system to suppress it. Indeed, HIV for research and as source of viral proteins for HIV-antibody tests is propagated in immortal lines of the very cell which, to cause AIDS, HIV is supposed to kill!--and in concentrations far higher than have ever been observed in any human, with or without AIDS.
AN EPIDEMIC OF AIDS TESTING
If HIV is virtually undetectable even in its alleged terminal victims, how do you test for it? You don't; you test for the antibody. What this means in principle is that a sample of the patient’s blood is exposed to viral antigens derived from HIV prepared in vitro. If the blood plasma contains antibodies to that antigen, they will bind to it in a reaction that can be made visible by suitable means, termed Enzyme-Linked Immuno-Sorbent Assay, ELISA, for those who love quoting these things at cocktail parties.
Wait a minute. . . . Aren't antibodies part of the body's own defense equipment--that you either acquired from your mother, learned to make yo urself at some time in life when you encountered the virus, or were tricked into making by a vaccine? If you have no symptoms of an illness and no detectable virus, but your system is supplying itself with antibodies, isn't this a pretty good description of immunity?
Yes--for any other disease, and if we were dealing with rationality. But this is the land of AIDS. The usual reason for antibody testing is as a check to see if somebody needs to renew their shots. Also, there are situations where testing for the antibody to a pathogen suspected of
14 Duesberg, 1992
causing a condition can make sense, given the right circumstances. If a person is showing clinical symptoms that are known to be caused by that pathogen (perhaps by satisfying Koch's postulates), and a test has been shown independently to identify an antibody specific to that pathogen, then testing for the antibody can be a convenient way of confirming the suspected disease without going through the rigmarole of isolation.
But none of this is true of HIV. It has never been shown to cause anything, nor has a likely explanation even been advanced as to how it could. What, then, if anything, does the "HIV test" mean?
A genuinely useful antibody test can confirm that an observed sickness is due to the microbe thought to be the culprit. A positive HIV result from somebody who is completely symptom- free, on the other hand, means either that the antibody has been carried from birth without the virus ever having been encountered, or that the virus has been successfully neutralized to the point of invisibility. So in this context, "HIV positive" means HIV-immune. Interpreting it as a prediction that somebody will die years hence from some unspecifiable disease makes about as much sense as diagnosing smallpox in a healthy person from the presence of antibodies acquired through childhood vaccination.
Testing for What?
The test can mean a lot of other things too. The most common, known as ELISA, was developed in 1984 for blood screening. Now, when you're looking for contaminated blood, you want a test that's oversensitive--where anything suspect will ding the bell. If the positive is false, after all, you merely throw away a pint of blood; but if a false negative gets through, the consequences could be catastrophic. (Whether or not what you're screening for is a real hazard isn't the issue here.) But the same test started being used for diagnosis. And when people are being told that a positive result means certainty of developing a disease that's inevitably fatal, that's a very different thing indeed.
Here are some of the other things that can give a positive result, which even some doctors that I've talked to weren't aware of: prior pregnancy; alcoholism; certain cancers; malaria antibodies; leprosy antibodies; flu vaccination; heating of blood sample; prolonged storage of the sample; numerous other viruses; various parasitic diseases; hepatitis B antibodies; rheumatoid arthritis. In fact, almost 70 other causes have been shown to be capable of causing a positive reaction that have nothing to do with AIDS conditions.15 In a mass screening in Russia in 1991, the WHO performed 30 million tests over a two-year period and found 30,000 positive results. Attempts to confirm these yielded around 300, of which 66 were actual AIDS cases.16
In addition to the tests being uncertain in that precisely what they measure has never been defined, and nonspecific in that many other factors can give the same result, they are not standardized. This means that no nationally or internationally accepted criteria exist for deciding what constitutes a positive result.
15 Ransom & Day, 2000, p.71; Maggiore 2000, p.11
16 Shenton, 1998, p.164
What people take as a death sentence on the basis of the things they've been told varies from one country to another, and even from one testing authority to another within the same country. The U.S. practice is to require a repeated positive result to an ELISA "Search" test, to be "Confirmed" by a test known as the HIV Western Blot (WB), which is supposed to be more accurate--although the UK won't use it because the risk of misinterpretation due to cross-reactions.
However, despite the reassuringly suggestive terminology, the WB remains as nonspecific, since it tests for the same antigen proteins as ELISA (but separated out into bands, so it's possible to see which ones are causing the reaction) and has likewise never been verified against any gold standard.17 In fact, some authorities cite it as the "standard" for assessing ELISA. This is a bit like using one clock to check the accuracy another, when neither has been verified to be correct in the first place. According to the WB interpretations handed down in different places, an HIV positive African would not be positive in Australia; a positive from the U.S. Multicenter AIDS Cohort Study 1983-1992 would not be positive anywhere else in the world, including Africa.18 The pamphlet supplied with the ELISA test kit from Abbot Laboratories states: "At present there is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood."
To add to this impact, my chosen career has developed around the HIV model of AIDS. I received my Ph.D. in 2002 for my work constructing mathematical models of HIV infection, a field of study I entered in 1996. Just ten years later, it might seem early for me to be looking back on and seriously reconsidering my chosen field, yet here I am.
As it turns out, the reason there was no consensus mathematically as to how HIV killed T-cells was because there was no biological consensus. There still isn’t. HIV is possibly the most studied microbe in history – certainly it is the best-funded – yet there is still no agreed-upon mechanism of pathogenesis. Worse than that, there are no data to support the hypothesis that HIV kills T-cells at all. It doesn’t in the test tube. It mostly just sits there, as it does in people – if it can be found at all. In Robert Gallo's seminal 1984 paper in which he claims "proof" that HIV causes AIDS, actual HIV could be found in only 26 out of 72 AIDS patients. To date, actual HIV remains an elusive target in those with AIDS or simply HIV-positive.
EXCERPT OF my personal experiences volunteering at an AIDS shelter in New Orleans for one week many years ago:
My personal experience with death was part of a student group going to a publicly funded HIV/AIDS shelter for the poor in New Orleans several years ago. Interestingly, the shelter was full of mostly elderly or middle-aged white people in apparently good health, even though the so-called AIDS & city demographics should be mostly young minorities. Anyway, when a person is diagnosed as having less than 24-hours to live (starts getting shakes in blinding pain, for example) the religious volunteers make sure that someone holds the hand of the dying person to "comfort" them until death; this period was called Vigil.
I saw a woman about 8-hours from death. She was white with a shaved head, and from the photographs in the room, appeared to be only in her 30s. Without the photos no one would know her real age. I don't recall seeing any family members. She was in blinding pain, with shakes, writhing sometimes. No other emotions or sign of human thought except pain.I was naive at the time, but I did think that the Vigil was more to make the volunteers feel better, because to the patient, it was all Senseless.
I had no idea at the time that the Medical Industry killed that woman with drugs to profit from a disease that she didn't have, a disease that may not even exist. Researchers like berkely prof Peter Duesberg had written this for years, only to get ostracized and funding cut. Assholes.
My guess now is that the smart ones didn't take their meds, just staying there for the free room & board.
A LIST OF HIV-AIDS SKEPTICS BOOKS from James P. Hogan's website:
www.jamesphogan.com/heretics/toc.php#aidsTHE TEXT OF two short letters from Duesberg , published in Science in 1988:
AIDS and the Ecology of Poverty by Eileen Stillwaggon (2005) -- Poverty and malnutrition as prime factors in Third-World AIDS
AIDS Cult, The by John Lauritsen and Ian Young (Eds.) (1997) -- Asklepios, Provincetown, MA, 1997. 224pp. ISBN 0-943742-10-2
AIDS War, The by John Lauritsen (1993) -- The subtitle: "Propaganda, Profiteering and Genocide from the Medical-Industrial Complex" says it all.
AIDS: A Second Opinion by Gary Null & James Feast (2001) -- An investigative reporter's comprehensive survey
Apocalyptics, The by Edith Efron (1984) -- A thoroughly researched revelation of how political ideology has corrupted cancer research in the United States.
Get All the Facts: HIV Does Not Cause AIDS by Mohammed Ali Al-Bayati (2002) -- Investigation and indictment of the effects of toxic antiviral drugs by a California-based pathologist, toxicologist, and AIDS dissident.
Infectious AIDS by Peter H. Duesberg (1995) -- A collection of thirteen articles originally published in scientific journals that call into question the dogma of infectious AIDS.
Inventing the AIDS Virus by Peter H. Duesberg (1996) -- A comprehensive case, presented by perhaps the most qualified and persistent challenger of the mainstream HIV theory of AIDS.
Myth of Heterosexual AIDS, The by Michael Fumento (1993) -- Dismisses the claim that was being repeated everywhere at the time of the book's publication that AIDS had "broken out" into the heterosexual population -- or that it ever would.
Oncogenes, Aneuploidy and AIDS by Harvey Bialy (2004) -- "A scientific life and times of Peter H. Duesberg." Harvey Bialy, himself a biochemist, interweaves the story of Duesberg's personal experiences with a broader view of how politics, money, vested interests, and an over-reliance by much of t
Origin, Persistence and Failings of HIV/AIDS Theory, The by Henry H. Bauer (2007) -- Irreconcilability of commonly held assumptions with the published data.
Poison By Prescription by John Lauritsen (1990) -- The AZT story
Positively False: Exposing the Myths Around HIV and AIDS by Joan Shenton (1998) -- Shows the HIV=AIDS=Death dogma which has wrongly acquired the force of certainty to be riddled with flaws.
Rethinking AIDS by Robert Root Bernstein (1993) -- A critical reappraisal of AIDS research that shatters conventionally unquestioned assumptions and reopens the fundamental questions of what is really known.
Science Sold Out: Does HIV Really Cause AIDS? by Rebecca V. Culshaw (2007) -- A mathematician's reasons for changing her position and quitting AIDS research
Serious Adverse Events: An Uncensored History of AIDS by Celia Farber (2006) -- Twenty years of reporting by a skeptical AIDS journalist
What If Everything You Thought. by Christine Maggiore (2002) -- A powerful deconstruction of the popular AIDS myths.
HIV Is Not the Cause of AIDS
By Peter H. Duesberg
Science, Vol. 241, pp. 514-517, July 29, 1988.
Human immunodeficiency virus (HIV) is not the cause of AIDS because it fails to meet the postulates of Koch and Henle, as well as six cardinal rules of virology.
1) HIV is in violation of Koch's first postulate because it is not possible to detect free virus (1, 2), provirus (3-5), or viral RNA (4, 6, 7) in all cases of AIDS. Indeed, the Centers for Disease Control (CDC) has established guidelines to diagnose AIDS when all laboratory evidence for HIV is negative (8).
2) In violation of Koch's second postulate, HIV cannot be isolated from 20 to 50% of AIDS cases (1, 9-11). Moreover, "isolation" is very indirect. It depends on activating dormant provirus in millions of susceptible cells propagated in vitro away from the suppressive immune system of the host.
3) In violation of Koch's third postulate, pure HIV does not reproduce AIDS when inoculated into chimpanzees or accidentally into healthy humans (9, 12, 13).
4) In contrast to all pathogenic viruses that cause degenerative diseases, HIV is not biochemically active in the disease syndrome it is named for (14). It actively infects only 1 in 104 to > 105 T cells (4, 6, 7, 15). Under these conditions, HIV cannot account for the loss of T cells, the hallmark of AIDS, even if all infected cells died. This is because during the 2 days it takes HIV to replicate, the body regenerates about 5% of its T cells (16), more than enough to compensate for losses due to HIV.
5) It is paradoxical that HIV is said to cause AIDS only after the onset of antiviral immunity, detected by a positive "AIDS test," because all other viruses are most pathogenic before immunity. The immunity against HIV is so effective that free virus is undetectable (see point 1), which is why HIV is so hard to transmit (9, 12, 13). The virus would be a plausible cause of AIDS if it were reactivated after an asymptomatic latency, like herpes viruses. However, HIV remains inactive during AIDS. Thus the "AIDS test" identifies effective natural vaccination, the ultimate protection against viral disease.
6) The long and highly variable intervals between the onset of antiviral immunity and AIDS, averaging 8 years, are bizarre for a virus that replicates within 1 to 2 days in tissue culture and induces antiviral immunity within 1 to 2 months after an acute infection (9, 17). Since all genes of HIV are active during replication, AIDS should occur early when HIV is active, not later when it is dormant. Indeed, HIV can cause a mononucleosis-like disease during the acute infection, perhaps its only pathogenic potential (9, 17).
7) Retroviruses are typically not cytocidal. On the contrary, they often promote cell growth. Therefore, they were long considered the most plausible viral carcinogens (9). Yet HIV, a retrovirus, is said to behave like a cytocidal virus, causing degenerative disease killing billions of T cells (15, 18). This is said even though T cells grown in culture, which produce much more virus than has ever been observed in AIDS patients, continue to divide (9, 10, 18).
8) It is paradoxical for a virus to have a country-specific host range and a risk group-specific pathology. In the United States, 92% of AIDS patients are male (19), but in Africa AIDS is equally distributed between the sexes, although the virus is thought to have existed in Africa not much longer than in the United States (20). In the United States, the virus is said to cause Kaposi's sarcoma only in homosexuals, mostly Pneumocystis pneumonia in hemophiliacs, and frequently cytomegalovirus disease in children (21). In Africa the same virus is thought to cause slim disease, fever, and diarrhea almost exclusively (22, 23).
9) It is now claimed that at least two viruses, HIV-1 and HIV-2, are capable of causing AIDS, which allegedly first appeared on this planet only a few years ago (20). HIV-1 and HIV-2 differ about 60% in their nucleic acid sequences (24). Since viruses are products of gradual evolution, the proposition that within a few years two viruses capable of causing AIDS could have evolved is highly improbable (25).
References and Notes:
- J. Albert et al., J. Med. Virol. 23, 67 (1987).
- L.A. Falk, D. Paul, A. Landay, H. Kessler, N. Engl. J. Med. 316, 1547 (1987).
- G.M. Shaw et al., Science 226, 1165 (1984).
- D. Richman, J. McCutchan, S. Spector, J. Infect Dis. 156, 823 (1987).
- C.-Y. Ou et al., Science 239, 295 (1988).
- M.E. Harper, L.M. Marselle, R.C. Gallo, F. Wong-Staal, Proc. Natl. Acad. Sci. U.S.A. 83, 772 (1986).
- A. Ranki et al., Lancet ii, 589 (1987).
- Centers for Disease Control, J. Am. Med. Assoc. 258, 1143 (1987).
- P.H. Duesberg, Cancer Res. 47, 1199 (1987).
- H. von Briesen et al., J. Med. Virol. 23, 51 (1987).
- D. Gallo, J. Kimpton, P. Dailey, J. Clin. Microbiol. 25, 1291 (1987).
- J.W. Curran et al., Science 239, 610 (1988).
- G.H. Friedland and R.S. Klein, N. Engl. J. Med. 317, 1125 (1987).
- J. Coffin et al., Science 232, 697 (1986).
- A. Fauci, ibid. 239, 617 (1988).
- J. Sprent, in B and T Cells in Immune Recognition, F. Loor and G.E. Roelants, Eds. (Wiley, New York, 1977), pp. 59-82.
- H.A. Kessler, J. Am. Med. Assoc. 258, 1196 (1987).
- R.C. Gallo, Sci. Am. 256 (No. 1), 47 (1987).
- Centers for Disease Control, AIDS Weekly Surveill. Rep., 18 April 1988.
- R. Baum, "AIDS: The molecular biology," Chem. Eng. News (23 November 1987), pp. 14-26.
- R.M. Selik, E.T. Starcher, J.W. Curran, AIDS 1, 175 (1987).
- R. Colebunders et al., Lancet i, 492 (1987).
- K.J. Pallangyo et al., ibid. ii, 972 (1987).
- F. Clavel et al., Nature 324, 691 (1986).
- J. Sonnabend, in New York Native (9 May 1988), p. 19.
Duesberg's Response to Blattner and Colleagues
Blattner, Gallo, and Temin defend the hypothesis that HIV causes AIDS only with epidemiology and anecdotal clinical cases in which AIDS is correlated with antibody to HIV, but not with active virus. I submit that this is insufficient because such evidence cannot distinguish between HIV and other causes, unless there is also evidence for biochemical activity of HIV in AIDS.
1 ) My opponents say that "following introduction of HIV in a population ... immunodeficiency emerges in a predictable sequence." Instead, epidemiological surveys show that the annual incidence of AIDS among persons with antibody to HIV varies from almost 0 to over 10%, depending on factors defined by lifestyle, health, gender, and country of residence (see point 8 of my preceding statement). Among antibody-positive Americans the avenge conversion rate is 1% [10,000 to 20,000 (1) of 1 to 2 million (2, 3)] but that of certain hemophiliacs (4) or male homosexuals (5) is 10% or higher. These discrepancies between the epidemiologies of HIV antibody and AIDS indicate that neither HIV nor antibody to it is sufficient to cause AIDS.
2 ) The argument that HIV, "not ... any other infectious agent," is linked to AIDS in blood transfusion recipients and in congenitally infected children is presumptuous for several reasons. Blood transfusion does not distinguish between HIV and "any other infectious agent" or blood-borne toxin. Further, it is presumed that the recipient had no risk factors other than HIV during the average of 8 years between HIV transfusion and AIDS symptoms. The transfusion evidence would be more convincing if AIDS appeared soon after a singular transfusion in generally healthy recipients. Transfusion AIDS cases, however, only occur very late after infection and mostly in persons with health risks, such as hemophilia, that are not representative of healthy individuals. Likewise, it is presumptuous to assume that HIV was the cause of AIDS in antibody-positive children, of whom 96% had other health risks, such as mothers who are prostitutes or addicted to intravenously administered drugs or blood transfusions for the treatment of hemophilia or other diseases (1, 6). The references to these cases would have been more convincing if antibody-negative controls had been included, having none of "the broad range of clinical diseases ... and the diversity of signs and symptoms of patients infected with HIV" (6).
3) According to authoritative sources, the primary defect of AIDS is a T cell deficiency induced by HIV infection (3, 7, 8). Therefore, it comes as a surprise that the primary clinical symptom of the children with AIDS was a B cell, not a T cell, deficiency (6). In fact, one of these same sources reports that "to fit observations from children into definitions for adult patients is unwise" (3). I wonder whether there is truly any disease that, in the presence of antibody to HIV, would not be called AIDS.
4) They claim that "interruption of HIV infection almost completely prevented the further appearance of blood-transfusion-associated AIDS." However, according to the CDC, transfusion-associated AIDS cases in adults have doubled to 752 cases and pediatric cases tripled to 68 in the year ending May 1988 compared to the previous year (1). This happened 3 years after antibody-positive transfusions were reduced 40-fold with the AIDS test (9). The steep increase in transfusion AIDS cases despite the great reduction of HIV-contaminated transfusions argues directly against HIV as the cause of AIDS.
5) In addition to the correlation that "in countries with many persons with HIV antibodies there is much AIDS," it is necessary to demonstrate some HIV-specific biochemical activity at the onset of AIDS to prove that HIV causes AIDS. All other viruses and microbes are very active when they cause fatal, degenerative diseases similar to AIDS. There is also abundant generic evidence that this activity is necessary for pathogenicity. Antibodies are evidence for the absence of an active virus, not a prognosis for future disease or death. Prior claims for etiology without genetic or molecular evidence for activity proved to be some of the most spectacular misdiagnoses in virology: (i) Based on epidemiological evidence, "scientists concluded" that Epstein-Barr virus was the cause of Burkitt's lymphoma-until the first virus-free lymphomas were found (10). (ii) On epidemiological grounds, human and bovine retroviruses were believed to cause leukemia after bizarre latent periods of up to 40 years in humans (11)-but finding these viruses in billions of normal cells of millions of asymptomatic carriers has cast doubt on this view (12). It is scarcely surprising that these leukemias arose from virus-infected cells. Consistent with this view, these "viral" leukemias are clonal and not contagious, behaving like virus-negative leukemias, and the associated "leukemia" viruses are not biochemically active (12). (iii) "Slow viruses" were accepted as causes of Alzheimer's, kuru, and Creutzfeldt-Jakob disease (13) on the basis of the same kind of epidemiology and transmission evidence used here for HIV-but these viruses have never materialized. These examples illustrate that correlations without evidence for biochemical activity are not sufficient to prove "etiology."
6) I fully support the view that "knowledge of the cause of a disease (etiology) is important for control." Since the cause of AIDS is debatable, the control of AIDS may not be achieved by controlling HIV. This is particularly true for the highly toxic "control" (preventive or therapeutic) of AIDS with azidothymidine (AZT)-AZT is designed to inhibit viral DNA synthesis in persons who have antibodies to a virus that is not synthesizing DNA (14).
References and Notes
- Centers for Disease Control, AIDS Weekly Surveill. Rep. (2 May 1988).
- W. Booth, Science 239, 253 (1988).
- Institute of Medicine, Confronting AIDS (National Academy Press, Washington, DC, 1986).
- M.E. Eyster, M.H. Gail, J.O. Ballard, H. Al-Mondhiry, J.J. Goedert, Ann. Int. Med. 107, 1 (1987).
- A.R. Moss et al., Brit. Med. J. 296, 745 (1988).
- B.E. Novick and A. Rubenstein, AIDS 1, 3 (1987).
- Centers for Disease Control, J. Am. Med. Assoc. 258, 1143 (1987).
- A. Fauci, Science 239, 617 (1988).
- J.W. Ward et al., N. Engl. J. Med. 318, 473 (1988).
- J.S. Pagano, C.H. Huang, P. Levine, ibid. 289, 1395 (1973).
- R.C. Gallo, Sci. Am. 255 (No. 6), 88 (1986).
- P.H. Duesberg, Cancer Res. 47, 1199 (1987).
- D.C. Gajdusek, Science 197, 943 (1977).
- D.D. Richoran et al., N. Engl. J. Med. 317, 192 (1987).
ABSTRACT OF DUESBERG'S 1987 REVIEW ARTICLE IN Cancer Research :
Retroviruses as Carcinogens and Pathogens:
Expectations and Reality
By Peter H. Duesberg
Cancer Research, Vol. 47, pp. 1199-1220,
(Perspectives in Cancer Research), March 1, 1987.
AbstractRetroviruses (without transforming genes) are thought to cause leukemias and other cancers in animals and humans because they were originally isolated from those diseases and because experimental infections of newborns may induce leukemias with probabilities of 0 to 90%. According to this hypothesis viral cancers should be contagious, polyclonal, and preventable by immunization. However, retroviruses are rather widespread in healthy animals and humans where they typically cause latent infections and antiviral immunity. The leukemia risk of such infections is less than 0.1% and thus about as low as that of virus-free controls. Indeed retroviruses are not sufficient to initiate transformation (a) because of the low percentage of symptomatic virus carriers and the complete lack of transforming function in vitro; (b) because of the striking discrepancies between the long latent periods of 0.5 to 10 years for carcinogenesis and the short eclipse of days to weeks for virus replication and direct pathogenic and immunogenic effects; (c) because there is no gene with a late transforming function, since all genes are essential for replication; (d) because host genes, which do not inhibit virus, inhibit tumorigenesis up to 100% if intact and determine the nature of the tumor if defective; and above all (e) because of the monoclonal origin of viral leukemias, defined by viral integration sites that are different in each tumor. On these bases the probability that a virus-infected cell will become transformed is estimated to be about 10-11. The viruses are also not necessary to maintain transformation, since many animal and all bovine and human tumors do not express viral antigens or RNA or contain only incomplete proviruses. Thus as carcinogens retroviruses do not necessarily fulfill Koch's first postulate and do not or only very rarely (10-11) fulfill the third. Therefore it has been proposed that retroviruses transform inefficiently by activating latent cellular oncogenes by, for example, provirus integration. This predicts diploid tumors with great diversity, because integration sites are different in each tumor. However, the uniformity of different viral and even nonviral tumors of the same lineage, their common susceptibility to the same tumor resistance genes, and transformation-specific chromosome abnormalities shared with nonviral tumors each argue for cellular transforming genes. Indeed clonal chromosome abnormalities are the only known transformation-specific determinants of viral tumors. Since tumors originate with these abnormalities, these or associated events, rather than preexisting viruses, must initiate transformation. Therefore it is proposed that transformation is a virus-independent event and that clonal viral integration sites are consequences of clonal proliferation of transformed cells. The role of the virus in carcinogenesis is limited to the induction of hyperplasia which is necessary but not sufficient for carcinogenesis. Hyperplasia depends on chronic viremia or high virus expression which are very rare in animals outside the laboratory and have never been observed in humans. Since latent viruses, which are typical of nearly all natural infections, are neither direct nor indirect carcinogens, they are not targets for cancer prevention. Viruses are also not targets for cancer therapy, since tumors are not maintained and not directly initiated by viral genes and occur naturally despite active antiviral immunity.
Lymphotropic retrovirus has been proposed to cause AIDS because 90% of the patients have antibody to the virus. Therefore antibody to the virus is used to diagnose AIDS and those at risk for AIDS. The virus has also been suggested as a cause of diseases of the lung and the nervous system. Promiscuous male homosexuals and recipients of frequent transfusions are at a high risk for infection and also at a relatively high annual risk for AIDS, which averages 0.3% and may reach 5%. Others are at a low risk for infection and if infected are at no risk for AIDS. AIDS viruses are thought to kill T-cells, although these viruses depend on mitosis for replication and do not lyse cells in asymptomatic infections. Indeed the virus is not sufficient to cause AIDS (a) because the percentage of symptomatic carriers is low and varies between 0 and 5% with the risk group of the carrier, suggesting a cofactor or another cause; (b) because the latent period for AIDS is 5 years compared to an eclipse of only days to weeks for replication and direct pathogenic and immunogenic effects; and (c) because there is no gene with a late AIDS function, since all viral genes are essential for replication. Moreover the extremely low levels of virus expression and infiltration cast doubt on whether the virus is even necessary to cause AIDS or any of the other diseases with which it is associated. Typically, proviral DNA is detectable in only 15% of AIDS patients and then only in 1 of 102 to 103 lymphocytes and is expressed in only 1 of 104 to 105 lymphocytes. Thus the virus is inactive or latent in carriers with and without AIDS. It is for this reason that it is not transmitted as a cell-free agent. By contrast, all other viruses are expressed at high titers when they function as pathogens. Therefore AIDS virus could be just the most common occupational infection of those at risk for AIDS because retroviruses are not cytocidal and unlike most viruses persist as latent, nonpathogenic infections. As such the virus is an indicator of sera that may cause AIDS. Vaccination is not likely to benefit virus carriers, because nearly all have active antiviral immunity.
ABSTRACT OF DUESBERG'S 2003 ARTICLE IN Journal of Biosciences:
The chemical bases of the various AIDS epidemics: recreational
drugs, anti-viral chemotherapy and malnutrition
PETER DUESBERG†, CLAUS KOEHNLEIN* and DAVID RASNICK
Donner Laboratory, University of California Berkeley, Berkeley, CA 94720, USA
*Internistische Praxis, Koenigsweg 14, 24103 Kiel, Germany
† Corresponding author
J. Biosci. 28 383–412
In 1981 a new epidemic of about two-dozen heterogeneous diseases began to strike non-randomly growing numbers of male homosexuals and mostly male intravenous drug users in the US and Europe. Assuming immunodeficiency as the common denominator the US Centers for Disease Control (CDC) termed the epidemic, AIDS, for acquired immunodeficiency syndrome. From 1981–1984 leading researchers including those from the CDC proposed that recreational drug use was the cause of AIDS, because of exact correlations and of drug-specific diseases. However, in 1984 US government researchers proposed that a virus, now termed human immunodeficiency virus (HIV), is the cause of the non-random epidemics of the US and Europe but also of a new, sexually random epidemic in Africa. The virus-AIDS hypothesis was instantly accepted, but it is burdened with numerous paradoxes, none of which could be resolved by 2003: Why is there no HIV in most AIDS patients, only antibodies against it? Why would HIV take 10 years from infection to AIDS? Why is AIDS not self-limiting via antiviral immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and Europe not random like other viral epidemics? Why did AIDS not rise and then decline exponentially owing to antiviral immunity like all other viral epidemics? Why is AIDS not contagious? Why would only HIV carriers get AIDS who use either recreational or anti-HIV drugs or are subject to malnutrition? Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs 7–9%, but that of all (mostly untreated) HIV-positives globally is only 1-4%? Here we propose that AIDS is a collection of chemical epidemics, caused by recreational drugs, anti-HIV drugs, and malnutrition. According to this hypothesis AIDS is not contagious, not immuno-genic, not treatable by vaccines or antiviral drugs, and HIV is just a passenger virus. The hypothesis explains why AIDS epidemics strike non-randomly if caused by drugs and randomly if caused by malnutrition, why they manifest in drug- and malnutrition-specific diseases, and why they are not self-limiting via anti-viral immunity. The hypothesis predicts AIDS prevention by adequate nutrition and abstaining from drugs, and even cures by treating AIDS diseases with proven medications.
This post was last edited 1/12/2008 at 2:11 P.M.