Document:Science fight

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NB: The full original debate, as it appeared in Science, can be found here.

My own response to Booth’s misleading reporting (3), which in a mangled account of the White House affair had mentioned my name, was a letter to Daniel Koshland, Science’s editor at the time, whom I knew a good deal longer and better than John Maddox, since he was one of my teachers in graduate school.

Koshland, unlike Maddox, is not only a scientist but one of considerable professional accomplishment. As I reminded him in my letter, in the late sixties he was the “Duesberg of allostery” when his own hypothesis about the way conformational changes in enzymes came about was almost universally considered to be wrong. I also chided him for allowing Fauci, Gallo, and Baltimore’s unbecoming, ad hominem attacks and personal insults. According to Peter, as a result of this letter and a few others – and, I think, a real sense of personal regret for not paying closer attention to what his journal was intending to publish – Koshland, who was commuting between his lab at Berkeley and a second office in DC (which perhaps explains his lapse in properly editing the Booth article), was sympathetic and accommodating when Peter reached him by telephone shortly after returning from the UK. The eventual outcome of their conversation was a “Policy Forum” that ran in Science the last week of July 1988 in which Duesberg and some of his principal opponents would finally begin an exchange of scientific arguments. Peter remembers its inception as follows:

Having been so “personally” represented by Booth/Science I insisted to Dan that I should be given adequate space to explain that, contrary to Booth, I was not without a cause, and what my “cause” was. Obviously Koshland/Science decided upon receipt of my piece making essentially the points of the later Policy Forum that so much anti-American HIV writing could not be presented to the readers without immediate “balance” by Blattner, Gallo & Temin. And that was Koshland’s Salomonic decision – we all could have our cake. I had my right of reply, Gallo had saved HIV for the “honor roll” of American science, and Dan was everybody’s friend.

Koshland told Duesberg that he wanted him to reduce the length of his piece to approximately five hundred words so that it matched the length of a statement making the case that HIV was the cause of AIDS he had received from William Blattner, Robert Gallo, and Howard Temin. Upon receipt of that he would send Duesberg Gallo’s piece (and vice versa) for an additional five hundred-word rebuttal, and the entire exchange would be published as a “Policy Forum.” Of all the puzzling features concerning Peter’s relentless and almost totally unsuccessful attempts to bring his considered and fully documented arguments to a wider scientific audience, the severe space restrictions that Science insisted on (and later Nature, as we saw in the previous chapter) is one of the more enigmatic, given the magnitude of the concern about AIDS and the fact that the same journals devote literally thousands of pages to the often much less considered words of the HIV orthodoxy.

Nevertheless, Peter complied, and after a certain amount of back and forth, in July “Koshland/Science” published what is still the only semblance of a real debate on the cause of AIDS in the scientific literature (8). That Howard Temin was the senior representative for the virus-AIDS proponents merits special attention, since Temin never worked on HIV, and Peter’s failure to do so was often used as a major hammer against him. But as I pointed out in the last chapter, Howard was the untarnished, undisputed champion of “new” when it came to retroviruses, and “new” as we will now see was to be the first line of defense of the virus-AIDS camp. In addition, neither Gallo nor Blattner (nor the two together) had the scientific credentials to stand against Peter unsupported nor, judging from their later writing, the skill to muster unassisted even the weak rebuttals to his five hundred prosecutorial words that appeared. Nobody I spoke to after the fact thought Gallo’s side had won. In keeping with the generally non-confrontational temperament of scientists, most were content to call it a draw, go back to their labs, and await further developments.

As in all debates, in the first round each opponent comes out with his or her best rhetorical flourish. And if I were judging, I would have to score the round 10–9 for Team Virus, since I believe Peter made a tactical error in setting an excessively didactic tone in his opening statement, giving the other side opportunities to feint and jab. I favored the “come out swinging,” experimental challenge style of the Bio/Technology “Last Word” and the summation paragraphs in Cancer Research. But Peter had his own ideas, and ignoring advice from his corner, began as follows: 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. (8)

The postulates for microbial disease causation originally formalized by the German microbiologist Robert Koch in the middle of the nineteenth century are familiar to every student of biology. They were established in order to correct a serious, unintended consequence of Pasteur’s essential proof of the germ theory of disease. Almost exactly like the mutant gene hunters of today, the new microbe hunters of Pasteur’s time were finding disease-causing microbes everywhere, and conditions from headaches to heartaches were being blamed on all sorts of bacteria with no attention whatsoever given to distinguishing a harmless passenger microbe from a pathogenic one. In stepped Peter’s hero Koch, who said it is only logical that any microbe proposed as a disease-causing candidate must satisfy the following conditions: It should be present in all cases of the disease from which it should be possible to isolate it in a pure form, and in such a pure form it should be capable of reproducing the disease in a susceptible host.

Whether or not HIV meets these criteria, there is no one who could counter that the postulates themselves are not standard textbook fare. The “six cardinal rules of virology,” however, are a different kettle of fish. There is no text that lists the rules of virology. What Peter, in deciding to play “Herr Doktor Professor” to the hilt, now called rules are really no different from the former experimental challenges. But being re-designated, their actual content was somehow diminished, and the Temin team used this dogmatic approach against the apparent iconoclast. Although failing to do any damage to the body, they could at least redden his face a bit by countering that “Biology is an experimental science and new biological phenomena are constantly being discovered.” (8)

In what follows, I comment on rounds one and two, combining them since it is only in the second round that a debate has any action. Peter followed his dogmatic one-two punch with a couple of sharp jabs, noting that detection and isolation of the virus from all AIDS cases had hardly been demonstrated as of mid-1988; and further, that isolation of HIV from AIDS patients depended on the laboratory activation of deeply asleep HIV genomes that at best resided in only 10–15% of the body’s white blood cells. This is a task that virologists of even the recent past would have found impossible. This second point is an important corollary of the key argument we examined in the previous chapter concerning the absence of sufficient active virus in AIDS patients to account for the collapse of their T-cell immunity. It is not enough to deflect the first punch, as Team Virus would, by saying that newer techniques, like more sophisticated versions of basic PCR, now did or would show that HIV proviral genes are present in “virtually all” AIDS patients, and then pretend that the second blow was never even thrown, let alone landed hard. Detecting a viral gene or genome is not the same as isolating a virus. If there is too little active virus present to be readily isolated, then its role as a causative agent is automatically suspect. As Peter continues to point out: “Even a post-modern virus should do something to get something done. HIV is biochemically so quiet it needs 35 cycles of PCR to hear it.” (8)

Kid Heretic followed his two stiff opening jabs with an uppercut that connected with enough force to reverberate loudly even today. Why don’t chimpanzees develop AIDS after experimental infection with HIV? They are, after all, our closest genetic relatives, and they are susceptible hosts for every single human virus, including HIV. And yet, today when more than fifty chimpanzees have been successfully infected for more than seventeen years, as demonstrated by their positive “AIDS-tests,” not one has developed clinical AIDS. There is no other virus that causes a disease in humans which will not reproduce that disease in chimps. Team Temin could only come back with: “It is true HIV does not cause AIDS in chimpanzees. Most viruses are species-specific in host range and in capacity to produce disease.” (8) Host range is not at issue since HIV infects chimps quite all right, but they follow this flay at thin air with a powerful-sounding near miss. “For example, herpes B virus, yellow fever virus, and dengue virus cause serious diseases in humans, but produce no disease symptoms during infection in many species of monkeys.” (8) Chimps may be a lot of things, but they are most definitely not monkeys, and every one of these viruses is pathogenic for them.

The virus corner then throws a thunderous boomerang punch. Temin’s team invokes the recently discovered simian immunodeficiency virus (SIV) and its equally new disease, Simian AIDS, to preserve Koch’s postulates, just as they would later trot forth the new feline immunodeficiency virus (FIV) and its brand-new disease, feline AIDS. Whether these animal models even resemble human AIDS – a topic we will visit in passing later on – the essential point is that we are now asked to believe one of two highly improbable alternatives: Either these latter diseases were present all along in monkeys and cats, and animal retrovirologists, as desperate as their human retrovirologist colleagues to find some clinical relevance for their work, had somehow missed them; or a whole bunch of new deadly retroviruses all evolved at the very same moment. Coincidentally, just in time to butter a lot of stale bread.

Peter flicks a few stinging, Ali-like jabs by asking the other side to reconcile devastating T-cell loss with minimal infectivity, biochemical quiescence, and with the presence of virus-inactivating antibodies. Not on the steadiest of legs, Team Virus shoots back with p24 antigenemia, and chronic herpes – the former to defend the preposterous notion that there were enormous amounts of active virus “hiding” (their word) in the body, and the latter to establish their point that “Many viruses are highly pathogenic after evidence of immunity appears.” Neglecting, of course, to mention that reactivated viral diseases like herpes and hepatitis occur only when the immunity gets low, are in step with easily detected virus production, and recede when the immune system responds. Not quite the scenario of HIV and AIDS.

The Duesenberger follows with a hard right to the head: HIV, in common with all other retroviruses, does not kill defenseless cells in culture. Why, therefore, should we imagine that it does so in the body when it is effectively neutralized by the host’s immune system and its tiny genome is sleeping peacefully in a highly evolved, complex community of cells that on rare occasions can even win a fight with rabies, until HIV the absolute deadliest of human viruses. This caused Team Temin, which should have been staggering on the ropes, to dig down and come up with an unexpected – and to almost everyone judging, strong – series of counter punches, although to this judge a lot of them seemed more phantom than ferocious.

For example, they claim several times that Peter is requiring the mechanism by which HIV kills cells to be delineated before it is accepted that it does. He is doing no such thing. He is saying, however, over and over again, that while knowing the mechanism by which a virus destroys cells is not necessary to establish causation in the case of a virulent, active virus, it is in the case of a mild-mannered fellow like HIV. Claiming that it kills legions of cells in the absence of a demonstrable mechanism is a lot like accepting the logic behind the story of the lion-killing bird that I heard from one of my Nigerian in-laws 25 years ago. It is well known that in the forests of West Africa there is a terrible yellow bird that can kill even the king of beasts. Although no one has actually observed this amazing feat, each and every time a dead lion is discovered, perched atop its once-proud head is the diabolical avian assassin. This parable, it should be obvious, is told to children as a caution against inferring cause from correlation.

Temin et al. go on to argue: “The exact mechanism of CD4 cell depletion in AIDS patients is not known, but several indirect mechanisms are known by which HIV can cause CD4 cell depletion in laboratory studies and could operate in vivo.” (8) Can and could, not does. But Team Virus now shifts from phantom punches and misleading adjectives like “exact,” which implies approximate knowledge not no knowledge at all, to low blows, saying that in fact HIV does directly kill cells in culture, and that Duesberg is as usual all wrong.

The very special kind of cell-killing they conjure is a transient, laboratory artifact called “syncytia formation” that, while relatively unknown to anyone outside the field, is common knowledge among retrovirologists. Because it appeared often in the defense of HIV between the years 1987 and 1993, and still surfaces on occasion when the asserter thinks he can get away with it, we will expend a little effort to examine it now.

When a retrovirus productively infects a cell – that is, actively directs the synthesis of new virus particles from its residence within the nucleus, which it can do maximally at about 1000 particles per day – the new viruses leave by insinuating themselves in and through the cell’s membrane. If such a virus-producing cell is in close proximity to uninfected ones, the sticky protein of the virus’ coat can glom onto the membrane of an adjacent cell, causing them to fuse. If enough cells fuse, a giant cell or syncytium forms, and the entire mass becomes unviable and dissolves. Thus apparent cell-killing by HIV. But this phenomenon depends on having infected and uninfected cells extremely close together, as they are in a tissue culture dish but not in the body, and on having just the right ratio of infected to uninfected cells. Once most of the cells in a population are infected, they are no longer fusible since there are no free surface receptors that can be used to make the virus cross-linked giant cell. And perhaps most damningly, fusion is only observed in the laboratory for the simple reason that it is completely inhibited by the antibodies present in the blood of infected people.

Peter would go on to deal with in vitro cell-killing by HIV, or more accurately the lack thereof, at much greater detail in the Proceedings review, but by then it was clear that no matter what holes were to be punched in the fabric of HIV-AIDS, it would magically heal itself and continue to wrap the entire globe in its satisfying warmth, a kind of medical Linus’ blanket for everybody.

The graying, middle-aged heretic delivered his last punch, a Joe Frazier left hook just as the bell sounded. It was effective then, and given the passage of time, even more so now when the genomic revolution has re-energized the biotechnology stock exchange. Thus finding similarities between genes in two organisms, which are taken to imply they do the same thing, or finding large differences between two gene sets, which means they are not likely to do the same things, can be worth mega-bucks. Peter connected solidly with: “It is now claimed that at least two viruses, HIV-l and HIV-2, are capable of causing AIDS, which allegedly first appeared on the planet only a few years ago (20). HIV-l and HIV-2 differ 60% in their nucleic acid sequences (24).” (9)

A wobbly Team Virus could only respond to this by reasserting the premise and waving their hands. “It is true that there are two viruses that cause human AIDS, HIV-l and HIV-2. The origin of these HIVs is an interesting scientific question that is not relevant to whether or not HIV causes AIDS.” (8)

Independent of their skill as counter-punchers, in their opening, the defenders of the faith came out cocky and styling. As well they could considering the evidence that HIV caused AIDS was “overwhelming” to the point of not even needing to respond to Dr. Duesberg, who while a “brilliant chemist, is out of his depth when it comes to biology and the complex interplay of the human immune system, which is still very much a black box in persons with AIDS,” according to an unspecified number of anonymous AIDS researchers quoted by Bill Booth in his provocative Science portrait(3). But curiously, as sharply as they posture, they do not produce the substance expected of eminent virologists tuned into the “complexities of the human immune system.” Quite the contrary, this hastily assembled A-team argues just like their poor-relation epidemiologists, who no matter what they would like to claim are glorified pollsters, not experimental scientists, and cannot prove functional hypotheses.

Kibbitz aside, Team Virus opens with: “AIDS, a new disease, was first recognized in 1981, clustered in male homosexuals, intravenous drug abusers, and hemophiliacs in the United States and among sexually active heterosexuals in some parts of equatorial Africa. Human immunodeficiency virus (HIV) was first discovered in 1983 and was definitively linked in 1984 to AIDS patients and to groups whose members were at high risk for developing AIDS.” (8) Quite a feat of recognition. I’m sure our Nobel-carrying and Nobel-aspiring team could have explained, if anyone had bothered other than Duesberg or a few nut-cases who supported his right to ask, exactly how they defined “sexually active heterosexuals in some parts of equatorial Africa,” and how they were so different from sexually active heterosexuals in the U.S. that their so-called brand-new AIDS diseases (which had long been present among sexually active and inactive hetero- and homosexuals all over Africa) could be so quickly distinguished, with such precise demography, years before the earliest antibody tests?

Somebody must have asked Cambridge University’s eminent virologist Abraham Karpas something similar, however, because not long after the debate, John Maddox (in his continued commitment to “not distress or mislead” but otherwise inform his large scientific readership by withholding and then refusing publication of Peter’s review) found he was compelled to publish a full page of “Scientific Correspondence” from Karpas explaining the origin of AIDS in Africa. Consider the ringing words of the distinguished don in which he displays the Sheffield razorsharp, critical acumen expected after a lifetime in the selfless service of Her Majesty’s science:

"The first plausible explanation for the origin of AIDS by cross-species transfer is due to Noireau in 1987 (ref. 11). He referred to a book published by Anicent Kashamura, a member of the Idjwi tribe of the Lake Kivu region in East Zaire. Kashamura deals with the sexual habits of the people of the large African lakes. Noireau quotes the following sentence: “To stimulate a man or a woman and induce them to intense sexual activity, male monkey blood for a man or she-monkey blood for a woman is directly inoculated in the pubic area and also into the thighs and back.” (ref. 12) Such practices would constitute an efficient means of trans-species transmission and could be responsible for the emergence of SIV infections of man and thus AIDS. (10)

Forgetting, if we can, this unashamed endorsement of bizarre sado-masochistic fanciful anthropology and racism by Sir John and his journal, and returning to the more refined arena of our interrupted mental boxing match, as a pedantic editor I might have intervened here with my red Pilot Point and eliminated some of the redundant “newness.” “Recognized in 1981” and “identified in 1983” are more grammatically correct and factual, if less insistent and evocative. But left unmarked, Team Tuned In lays it on as follows:

“The strongest evidence that HIV causes AIDS comes from prospective epidemiological studies that document the absolute requirement for HIV infection for the development of AIDS. It has been shown for every population group studied in the United States and elsewhere that, in the years following the introduction of HIV and subsequent seroconversion of members of that population, the features characteristic of progressive immunodeficiency emerge in a predictable sequence resulting in clinical AIDS (2–4).” (11)

Only if saying so makes it so, counters Kid Heretic. The references to their first ponderous claim are in fact no more than previous assertions of the same thing, not experimental studies that support it. Actual epidemiological surveys showed, and continue to show, that the occurrence of AIDS based solely on the detection of antibody to HIV is unpredictable in time of onset and in clinical manifestations, which are diverse and constantly changing. The onset of AIDS “varies from almost 0 to over 10%, depending on factors defined by life-style, health, gender, and country of residence (see point 8 of my preceding statement, and references therein).” (8) And one could add now the date of diagnosis, since the CDC has changed the definition of the “disease” several times over the years, just as the incubation period of the virus mysteriously adjusted itself from two to five years to ten to fifteen in order to reconcile epidemiological predictions with the actual numbers of new cases within particular intervals (12)

Ducking and weaving, the dauntless defenders try to double-up on their next big punch. “Support for the linkage of HIV infection and AIDS comes as well from the results of public health interventions where interruption of HIV infection almost completely prevented the further appearance of AIDS in blood transfusion recipients (4).” (13) And just a hundred words later: “As a result of the decrease in blood transfusion-associated transmission of HIV, the incidence of blood transfusion-associated AIDS among U.S. newborns showed a decline (4).” (13) Duesberg, looking a little exasperated, resorts to the same quantitative counter: “According to the CDC, transfusion-associated AIDS cases in adults have doubled to 752 cases and pediatric cases tripled to 63 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),” (14) citing James Ward and a large number of colleagues from the CDC’s AIDS Program in the February 1988 New England Journal of Medicine.

Having thrown these set-punches, Team Virus lets fly with their best shot:

“Scientists conclude that a virus causes a disease if the virus is consistently associated with the disease and if disruption of transmission of the virus prevents occurrence of the disease. HIV can be detected by culture in most AIDS patients and by culture or polymerase chain reaction in most HIV seropositive individuals (8, 9). Epidemiological data show that transmission of HIV results in AIDS and blocking HIV transmission prevents the occurrence of AIDS. Thus, we conclude that there is overwhelming evidence that HIV causes AIDS”. (15)

They finish with a dazzling display of fearless footwork: “Knowing the cause of a disease does not mean that there is complete understanding of its pathology. Discovering the pathogenetic mechanisms of HIV in AIDS is a major focus for research.”

After the “Policy Forum” appeared, Peter all but begged Dan to sanction another round, to no avail. And so just when it was getting good, the bout was declared a technical draw on an inexplicable and non-appealable decision of commissioner Koshland. There was never to be a rematch. The failure to extend the discussion in the pages of Science was significant. Most scientists have neither time nor inclination to follow specialist literature in fields outside their own. They depend, consequently, on journals like Science and Nature to tell them what is considered important. Having read, as best they could at the time, the arguments of the Policy Forum, and then seeing nothing more than vulgar anti-Duesberg editorials in the scientific press and worse in the popular media, even a partially persuaded non-specialist could and would eventually concur with the “overwhelming evidence” of Team Virus, although it has become even less overwhelming now than it was in 1988 (12).

But even this highly circumscribed exchange was not exactly what its editors pretended it was. In 1994, Peter received an anonymous fax from someone at the NIH giving a fuller picture of the team effort in Science. Among other revealing documents from the word processor of Florence Karlsberg, public relations officer of the NIH, was a memo from December 1987 addressed to top NIH officials stating that: “Alas – in the past few months, inquiries have been mounting... The calls and interest are mounting. Perhaps it’s time to review and activate the attached STATEMENT.” (16)

The loud statement had a curiously reminiscent title, “HIV: The Cause of AIDS,” and bore an uncanny similarity to the words of Team Virus six months later. As well it should since other documents in the fax showed that the statement had been written by William Blattner, months before Koshland received it with Gallo’s and Temin’s additional signatures. It was apparently composed in response to a request from the PR maven to “create a response team to deal with the controversy.” Karlsberg had suggested that “Perhaps the epidemiological approach might be more productive in countering Peter’s assertions.” (16) To switch from boxing to another metaphor from the sporting life: Talk about a stacked deck. The memos also explained why the piece in Science, despite having Temin as senior author, had none of his style, which was much more Duesberg-like and substantive than the government-ordered fluff to which he added his otherwise excellent name.

While this very peculiar “Policy Forum” was unfolding, Peter engaged in a fruitless attempt to get Nature to take action on his review. During the months the paper sat on Maddox’s desk, presumably inspiring the brilliant language of the letter that began this chapter, Peter spent more than a few hours readjusting the formatting on his Xerox computer, added material that addressed the unfinished points of the Policy Forum, and sent the manuscript to the Proceedings of the National Academy. As an Academy member, and therefore entitled to unfettered access to its journal, Peter thought this would be an easy publication, and while not nearly as visible or influential as either Nature or Science, it would at least set down his continued analysis for the attention of history, if not that of his apparently uninterested retrovirologist colleagues.

It was, in fact, to be the beginning of what Peter now calls “Duesberg apartheid on the part of the Proceedings,” since he would go from a perfect twenty-five-year record of thirty-four first-round acceptances to special reviews and rejections. Over the next months, the manuscript was summarily returned as being “unoriginal” by one editor, Maxine Singer, (16) and then resubmitted with protest to her successor Igor Dawid, where it generated more than sixty pages of correspondence between Dawid, Peter, and three anonymous reviewers before it was finally accepted in November (16) The point of this chronicle is not to show that Peter was being unfairly treated, which he may have been, but rather to underscore that the paper was published only after the most intensive scrutiny, and therefore its conclusions cannot be flippantly dismissed.

When the review did appear, with the title “Human immunodeficiency virus and acquired immunodeficiency syndrome: relation but not causation,” it was accompanied by an extraordinary and unprecedented “disclaimer” promising a rebuttal that was to be prepared by Robert Gallo. But when Peter or I asked him at various times over the next years how the refutation was coming, he was always “too busy saving lives to respond.”

References

3. Booth, W., 1988. "A rebel without a cause of AIDS", Science, 239: 1485-1488.

8. Duesberg, PH, "HIV is Not the Cause of AIDS"; and Blattner, W., Gallo RC, and Temin HM, "HIV is the Cause of AIDS", 1988. Science, 241: 515-517.

9. Ibid. References therein:

20. R. Baum, "AIDS: The molecular biology", Chem Eng News (November 23, 1987): 14-26.

24. F. Clavel et al., Nature, 324, 691 (1986).

10. Karpas, A., 1990. "Origin and spread of AIDS", Nature, 348: 578.

11. Noireau, F., Lancet 1 (8548): 1498-1499, 1987.

12. Kashamura, A. Famille Sexualite et Culture., Paris, 1973.

11. Blattner, W., Gallo RC, and Temin HM, "HIV is the Cause of AIDS", 1988. Science, 241: 515-517. References therein:

2. J. W. Curran et al., Science, 239, 610 (1988).

3. P. Piot et al., ibid., p. 573.

4. J. J. Goedert and W. Blattner, in AIDS: Etiology, Diagnosis, Treatment, and Prevention, V. T. DeVita, S. A. Rosenberg, S. Hellman, Eds. (Lippincott, Philadelphia, 1988). This decline in pediatric AIDS became evident before that in adult AIDS because of the shorter latent period for AIDS in infants.

12. Duesberg, PH, Koehnlein, C., and Rasnick, D, 2003. "The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy, and malnutrition.", J Biosci, 28: 383-412.

13. Blattner, W., Gallo RC, and Temin HM, "HIV is the Cause of AIDS", 1988. Science, 241: 515-517.

4. J. J. Goedert and W. Blattner, in AIDS: Etiology, Diagnosis, Treatment, and Prevention, V. T. DeVita, S. A. Rosenberg, S. Hellman, Eds. (Lippincott, Philadelphia, 1988). This decline in pediatric AIDS became evident before that in adult AIDS because of the shorter latent period for AIDS in infants.

14. Duesberg, PH, "HIV is Not the Cause of AIDS"; and Blattner, W., Gallo RC, and Temin HM, "HIV is the Cause of AIDS", 1988. Science, 241: 515-517. References within the Duesberg response:

1. Centers for Disease Control, AIDS Weekly Surveill. Rep. (May 2, 1988).

9. J. W. Ward et al., N Eng J Med, 318', 473 (1988).

15. Blattner, W., Gallo RC, and Temin HM, "HIV is the Cause of AIDS", 1988. Science, 241: 515-517.

8. S. Z. Salahudding et al., Proc Natl Acad Sci USA, 85, 5530 (1985).

9. C.-Y. Ou et al., Science, 239, 295 (1988).

16. Duesberg, PH, 1996. Inventing the AIDS Virus, Regnery Publishing, Inc., Washington DC.

© 2004 by Harvey Bialy
excerpt from Oncogenes, Aneuploidy, and AIDS