This has not occurred. It has been suppressed. Almost three more years have gone by. No error has yet been pointed out in my arguments, and the several attempts that have been made have been altogether pathetic. This current piece is, first and foremost, a thorough analysis of the most significant of these attempts.[3] This attempt, by the man whose vaccine is alleged to have started the AIDS epidemic, gets every single substantive point wrong.
For those unfamiliar with my arguments, I present a summary:
The vaccine in question, the first live oral polio vaccine ever given in a mass trial, was produced by Hilary Koprowski at the Wistar Institute in Philadelphia, USA, but the trial was not conducted anywhere in the medically advanced world. It was conducted in Central Africa, specifically in Eastern Zaire and adjoining Ruanda-Urundi (now Rwanda and Burundi), in 1957-58, and, a few months later, in Kinshasa, Zaire, more than 900 miles further west. The former site is the Lake Victoria area of Africa, which has the world's highest HIV rates and which had already been pinpointed by many researchers as the likely origin point of AIDS, based on purely epidemiologic reasons. The latter site, Kinshasa, is the location of the world's first clearly HIV-positive human blood sample, showing HIV antibodies by three independent tests, which sample was taken in 1959, the year after the vaccination campaign was conducted there.[4]
Contamination of oral polio vaccine with various simian viruses was extremely common, the most notorious incident being the contamination of many batches of both oral and killed (Salk) polio vaccine with live, infectious SV-40 virus from the rhesus and related monkeys whose kidneys were used to grow the polio virus from which the vaccines were made.[5] Millions of people were infected with this monkey virus, which, fortunately, was a great deal less deadly than AIDS. Koprowski himself speculated that a careful search might turn up foreign viruses in all live polio vaccine preparations.[6] Indeed, Sabin found a contaminating virus (which was never identified and is now apparently lost) in the very vaccine made by Koprowski and used in his African campaign.[7]
In the case of live virus vaccines grown on animal tissue, there is no way to kill contaminating animal viruses without at the same time killing the special non-pathogenic viral strains that constitute the vaccine, so that live virus vaccines are completely dependent on detection and disposal of contaminated batches before they are administered. For some contaminating viruses, detection may work. For unknown viruses, or known viruses that are difficult to detect, this is a hopeless task. Despite the fact that HIV was known to have contaminated many batches of the clotting factor used by hemophiliacs (from the bald fact that the majority of US hemophiliacs became infected with HIV), the most sensitive tests failed to confirm its presence, despite many attempts by many investigators over several years. In a massive 1993 review article containing 1340 references, Jay Levy writes (p. 191): "Nevertheless, evidence of virus particles in old clotting-factor preparations has just recently been substantiated by PCR analysis.... Attempts to isolate infectious HIV from these sources have thus far been unsuccessful."[8] The extraordinarily-sensitive PCR test was not available until a few years ago. Moreover, since it requires the DNA sequence of the virus, or an approximation to it, it only works for known viruses, or viruses related to known viruses, while neither HIV nor any of its SIV relatives was discovered before 1983. Even knowing particular batches of clotting factor were contaminated with a known virus did not enable even careful scrutiny by modern researchers to detect the virus for several years. To suppose that 1950s and 1960s researchers might have eliminated every batch of SIV-contaminated vaccine, which virus they did not know existed, using the far more primitive technology of the day, on the thousands of batches that were made, is absurd in the extreme. Sometimes the human race provides a far more sensitive culture medium for the detection of new viruses than any alternative test.
SIVs have been found in every one of the three monkey species commonly used for vaccine manufacture. One of these, an SIV of sooty mangabeys, was inadvertently transferred via scientists into rhesus and cynomolgus monkeys in primate colonies in the US. The scientists did not realize what had happened until many of these monkeys had died of a disease with symptoms strikingly reminiscent of AIDS, and indeed did not realize it even then until they had also inadvertently transferred AIDS into humans and thus had something similar to compare the monkey disease with, and in addition had the incentive to look into it more carefully. This SIV is almost identical to HIV-2, the other major form of AIDS, still mainly confined to West Africa. Polio vaccine was made from both rhesus and cynomolgus monkeys, and could therefore have been the origin of HIV-2 as well as of HIV-1. However, there are several other possibilities for the vaccinal origin of HIV-2, some of which explain much better the epidemiology. No one has looked very carefully into these various possibilities for the origin of HIV-2.
African green monkeys are the third species used for polio vaccine manufacture. Approximately one-third to one-half of all African green monkeys are infected with their own variety of SIV. However, it is clear from DNA sequence analysis that this variety of SIV was not the origin of either HIV-1 or HIV-2. SIV varieties vary enormously in their ability to infect other species, and apparently this particular variety cannot infect human beings, or can do so only with great difficulty, for otherwise we would be infected with it too. This does not preclude the possibility that there is a second, much rarer, SIV in green monkeys (or rhesus or cynomolgus monkeys or in one of the several other species that have occasionally been used to manufacture vaccine), and that this second SIV is much more closely related to HIV-1, and was, in fact, its ancestor. Indeed Lecatsas and Alexander think they may have found such an SIV in a single African green monkey,[9] though to my knowledge they have not yet confirmed it. There is also an SIV of chimpanzees that is much more closely related to HIV-1 than any of the known monkey SIVs. Since Koprowski started a chimpanzee colony in Africa and killed and dissected at least 10 chimpanzees in experiments leading to the production of the vaccine for the African campaign,[10] the contamination could have come from chimpanzee SIV instead of monkey SIV, and indeed, in my opinion, a chimpanzee virus is the most likely progenitor.
DNA sequence evidence indicates all HIV-1 strains trace their origin to a single case, which existed presumably in a single simian, who transferred it into the human race sometime around 1958 in Central Africa. My explanation is that the transfer occurred when this simian's virus got into Koprowski's vaccine and infected a (probably small) portion of the 300,000 people who were given it. The standard explanation is that the simian bit, or was eaten by, or killed by, a single individual who became infected and spread the virus to others. It is hard, but not impossible, to see how a single human infection could have grown so quickly into the worldwide epidemic. In any event, there is no direct evidence of any human case anywhere in the world before 1959, while the theoretical evidence (arrived at through comparison of modern strains and therefore not dependent on old stored samples) is in close agreement, pointing to roughly 1958.[11]
Regardless of how HIV got here, the epidemic that followed is due to the person-to-person spread of this virus around the world. According to my scenario only the initial cases in Africa received infected vaccine. The worldwide pandemic is due to each HIV-infected person infecting others. Had there been many batches of infected vaccine, there would not be a single origin in a single simian about 1958. Cases arising from every separately contaminated batch of vaccine would point to a different simian individual and to the approximate date that particular batch was administered. [This is an important point: please read the last two paragraphs again if you did not clearly understand it. And indeed, just a few weeks after writing those words, I learned of strong new evidence for a second, independent transfer of another strain of HIV-1 in or near Cameroon. The evidence is of exactly the sort mentioned in this paragraph. The information is discussed at some length in an Addendum, so bear in mind that my claims of a single contaminated batch are outdated and will be corrected in the Addendum.]
This single origin would be somewhat surprising had the virus come from the common SIV of green monkeys. Since such a large proportion of green monkeys are infected, and since thousands of them have been used to make thousands of batches of live polio vaccine, one would at first thought presume that there would be a great many points of origin and that various families of cases would trace their infections back to a great many monkeys, instead of just a single one. However, this gives too little weight to the fact that it is clearly difficult to transfer this virus into humans, since we have tried the experiment thousands of times without any transfers being detected so far. Therefore, it could have been a one-time event. Indeed, it may yet, one day, be a one-time event if we continue to use these monkeys in vaccine manufacture. HIV-1 has developed an enormous amount of variability in the less than four decades since its transfer. The natural SIVs of simians, having had far longer to diverge, are much more variable. To conclude that among this vast diversity existing in African green monkeys, only a small portion of which have we sampled, there is no single strain that can successfully infect humanity, would be a vastly premature conclusion. In my own opinion, it would also most probably be a wrong conclusion. I think it is rather likely that such variants exist and, if the experiment continues, that such a variant will ultimately be found.
A single origin would of course not be surprising if HIV-1 came from a second, far rarer SIV of green monkeys, such as Lecatsas and Alexander may have found, since it might have managed to contaminate only a single batch of vaccine owing to its rarity. Similarly, if the origin were contamination due to chimpanzee virus from dissected chimpanzees, this might well have been a one-time event, especially since relatively few chimpanzees are infected with the virus. Chimpanzee kidneys have never, to my knowledge, been used to manufacture any vaccine (though, as discussed below, Koprowski's statements of what simians he used have been both self-contradictory and contrary to biological fact; the species used was surprisingly not mentioned in any of the contemporary publications describing Koprowski's African vaccine, and it remains unknown today).
In 1991 virologist Robert Bohannon grew suspicious of polio vaccine (after finding a non-HIV, non-SIV monkey immunodeficiency virus in one of his AIDS patients who had had no known contact with monkeys, other than vaccination[12]) and proposed to test vaccine samples for HIV and related retroviruses. Wistar Institute and the FDA have used every imaginable means, from ignoring his letters to saying legal departments advised against it to saying the vaccine samples had been lost, in order to block his getting any sample of the African vaccine.[13] Moreover, various people, including Albert Sabin,[14] have made the extraordinary claim that it won't mean anything even if the virus is found in the vaccine, since stomach acid would have destroyed the virus before it could infect. (The epidemic could have been started by only a very few of the 300,000 Africans fed the vaccine becoming infected; New England Journal of Medicine found breast milk transferred infection to 4 of 11 infants whose mothers were not infected until after delivery.[15])
In October 1992, a panel of six "independent" experts hand-picked by the Wistar Institute produced a 2600-word exoneration of Wistar's vaccine.[16] With but one exception, the piece did not document a single one of their claims (their sparse documentation was confined to points that were not in dispute), some of which claims contradicted published accounts. The single exception was their citation of a five-paragraph letter to the journal AIDS, in which Japanese researchers (Ohta, et al.[17]) claimed to be unable to detect the SIV of African green monkeys in the kidneys of two infected African green monkeys and to be unable to grow it in the kidneys of two uninfected African green monkeys. I found eight separate fatal errors in this short paper[18] [plus other major non-fatal errors, such as an earlier paper by the same researchers (and one member of the Wistar Committee) saying that African green monkey SIV would not grow in the cell cultures they said in their five-paragraph letter they had used in their attempt to detect it].
Nevertheless, the hand-picked Wistar panel of experts recommended testing old samples of vaccine (to leave no stone unturned) and recommended polio vaccine no longer be made from monkey organs. The second recommendation has not been put into effect. I have heard a single unconfirmed report from a confidential but probably reliable source that Wistar did turn some vaccine material over to the CDC for testing. I have not heard any report of results. It is to my mind almost inconceivable that Wistar would have turned over any material it had not already tested itself and found clean. There is no clear way to determine whether vaccine turned over was the actual vaccine used in Africa, or some other batch. The CDC, moreover, has been among the most vocal critics of the polio vaccine theory. The Wistar panel of experts recommended the CDC as one of the two laboratories that should be given samples for testing (the other being the WHO, another of the vaccine theory's most vocal critics). Wistar panel member David Ho recommended Bohannon not be given any vaccine for testing.[19] It is to my mind almost certain that test reports on any vaccine samples that may have been turned over will be negative. Anyone who thinks -- after all the efforts that have been made to block testing, or to allow only opponents of the theory to test it, or to claim that it will be meaningless even if HIV-1's ancestor is found there -- that a negative result, coming after the various interested parties have had several years to substitute one batch for another or to otherwise cook the tests, will prove anything is exceedingly naive. The last time researchers attempted to test for SIV in vaccine manufacturing material, they committed eight fatal errors in their efforts to show it was not there. Those were only the errors that they published in the literature. Perhaps that is why this test, if it is occurring at all, is so much less public.
As for the Wistar Committee report, the eminent Oxford biologist WD Hamilton called it "so weak as to seem almost positive evidence in itself."[20]
In August 1992 Hilary Koprowski wrote a letter to Science in which he defended his vaccine against charges it had started AIDS.[3] The charges he chose to defend against were not those of my earlier work, finally published by the University of Wollongong in late 1991. Instead, Koprowski's letter attacked the independent work of investigative journalist Tom Curtis, published early in 1992 in Rolling Stone,[21] which was based on the ideas of AIDS activist Blaine Elswood, who came to conclusions very similar to mine, but who was unaware of my work because from late 1987 until December 1991, I had been unable to get it published.
Koprowski's defense contained at least 6 serious errors, plus 3 more that were less serious. More importantly, it did not contain a single significant point that was correct. Even the one clear (but insignificant) mistake he successfully pointed out in Curtis' piece did not apply to my own account.
Many of Koprowski's errors were so gross that Science also should be held to account for publishing them. Yet Science refused to publish Curtis' rebuttal, in which he clearly pointed out many of these errors, some of which, such as gross errors in map distances, were completely indisputable. Moreover, Science again refused to publish a letter from WD Hamilton, one of the foremost evolutionary biologists in the world, which asked only that this theory be looked into rather than suppressed. In an appendix not for publication, Hamilton pointed out 12 errors in Koprowski's letter to Science. (These were in fact the same errors I had found, but he counted them differently.) Science refused to publish this letter from a world-renowned biologist on a question on which hundreds of millions of lives depend, saying they had already published enough on the topic. They made no effort to deny any of the 12 errors Hamilton had pointed out. The argument appears to be that if you print a large enough volume of lies and errors, then you can claim to have printed enough on a subject and are excused from printing any corrections or considering the matter further.
The point of the present document is to clearly point out the various errors in Koprowski's letter, and, more importantly, to show that there was not a single point of significance that Koprowski got right. To point out errors, even many errors, does not constitute a refutation, unless one shows that one or more of them, separately or in concert, are fatal errors. On the other hand, to show that every significant point was in error surely constitutes the strongest possible refutation.
The following points are almost all taken from correspondence sent to several different people in the weeks after Koprowski's letter appeared. I had not previously combined them into a single document suitable for distribution. I have, I think, been scrupulously careful to document all controversial points. In addition, many of the uncontroversial points (standard information about HIV, etc.) have been documented, but I have been less careful here, presuming some background in my audience. Those with no background whatever can still read it profitably, as the missing documentation is nonessential. Most of it is supplied in one or both of my earlier pieces, What Happens When Science Goes Bad,[1] and "Preliminary Notes Concerning Shortcomings of a Correspondence by Y. Ohta, et al."[18] These three pieces fit together nicely. The current one probably fits best in the middle.
Going through the text, we encounter reference numbers in the order listed below. Whenever the number is correct, it stands alone. Whenever it is incorrect, it is followed by the number of the footnote that in fact corresponds to the reference number. (1), (2,11), (2), (1), (1), (3), (4), (4), (5), (6), (7), (5), (8), (9), (10), (11), (12), (11,13), (12,14), (13,15), (14, 16), (15,17), (16,18), (12), (17,19), (18,20), (19,21), (20,22), (21,23), (8), (23,24), (23,24), (2), (24,25). In the text, there is no reference 22 or 25.
It is seen that 34 reference numbers appear in the text (some multiple times) and 15 of these are incorrect.
Koprowski uses the following points against Curtis. This is an exhaustive list. [It will help to have read Koprowski's letter, and to have it before you as you proceed.]
(1) Curtis "has stated that the area of vaccination of children in Ruzizi Valley in 1958 corresponds `roughly to another map... the one identifying the regions of highest HIV... infection in equatorial Africa'.... This is completely wrong. Ruzizi Valley, where 215,504 subjects were vaccinated in 1958, is located in the northwestern part of the Republic of Burundi, not in the Kivu district of Zaire, an area where Curtis placed `the lion's share'" of the vaccinations.
(2) The earliest African cases were diagnosed several thousand km away from the Kivu region.
(3) The incidence in rural areas of the vaccine region is .7 or 1.3 or 3.7 percent. "If the AIDS virus had been administered to children in Burundi in 1958 through polio vaccine immunizations, would not a much higher percentage of infected adults than 0.7% be observed in rural areas? Yet it is the urban area in which the population is heavily (25 to 30%) infected with HIV, and it would seem that the spread in Africa occurs from urban areas to rural areas, not vice versa."
(4) Poland, given the same pool of vaccine, has the lowest AIDS incidence in Europe.
(5) The first proved case of AIDS was in a British sailor who died in 1959.
(6) The sailor was showing AIDS symptoms throughout 1958, before any mass vaccination was begun.
(7) The only monkeys Koprowski used for making vaccine were rhesus monkeys captured either in India or the Philippines. "India's ban on the shipment of their monkeys outside India did not affect delivery from the Philippines."
(8) It has been shown that green monkey kidney tissue from SIV-infected monkeys does not contain SIV.
(9) Sabin did not test the Congo vaccine but a seed lot of virus. And Koprowski's laboratory and two other laboratories could not find the contaminating virus Sabin says he found.
(10) Large numbers were vaccinated with CHAT (Koprowski's vaccine for type 1 polio) in Poland, Switzerland, and Croatia without starting AIDS epidemics there.
(11) "Curtis does not distinguish between lots of vaccines and seed lots of virus. There is no vaccine stored at the Wistar Institute."
(12) "Careful follow-up observation has proved the vaccine to be safe and unassociated with any major illness." "Again, there was no doubt about the safety of the vaccine because there were no untoward reactions that could be attributed to an extraneous agent." "The argument for the safety of polio vaccination lies in the absence of any AIDS-related disease among the hundreds of millions of people vaccinated throughout the world."
(13) "Curtis refers to the `high prevalence of antibodies'... in the Kivu district." But the authors of the report Curtis used for this information later decided their high incidence was due to false positives, which the first generation of tests was much subject to.
This last criticism is valid, and Curtis has retracted this claim. It is an unimportant retraction, because everyone agrees that once false positives are eliminated, the area of Central Africa, where the vaccine was administered, still has highest HIV rates in the world.
All the other criticisms, except for a couple of points too minor to count, consist of errors on Koprowski's part.
Commenting on the others, in order:
(1) Koprowski may be correct that Curtis erred in placing the lion's share of the vaccinations in the Kivu district. The Ruzizi river is the boundary between Burundi and the Kivu district of Zaire. The maps of the vaccination sites are not detailed enough to tell on which side of this river the majority of the Ruzizi Valley vaccinations occurred. At most, the error consists of placing the location on the wrong side of a river. The town (Katana) of the Kivu district in which the high seropositivity was detected, lies just north of Bukavu, and is roughly 30 miles, or 48 km, from the Ruzizi valley, site of more than 200,000 vaccinations. To call this "completely wrong" is a gross exaggeration which obscures the close geographic proximity to the vaccinations. The point is moot, however, since admittedly the data finding high seropositivity in Katana were subsequently called into question, a fact Curtis was unaware of when he wrote. The entire Kivu district, as well as the area of northwestern Burundi where Koprowski says the bulk of the vaccinations occurred, is within the area of the map Curtis cited as giving the region of highest AIDS incidence. This map covers a fairly large area, but it still comprises less than 6.5% of the continent of Africa[23] -- less than 1.3% of the land area of the earth -- and this geographic coincidence is made more impressive by the fact that the area of greatest vaccination lies very near the center of the map. This map, and many similar maps concentrating on the Lake Victoria region of Africa, are widely acknowledged as giving the region of highest incidence, and for Koprowski to call Curtis' geographic data "completely wrong" because the location was a few miles off and because the incidence in the particular town he cited had been scaled back, when no one questions the high incidence in the map area overall, is a gross distortion.
(2) The first AIDS case listed in the source Koprowski cites was in Kinshasa, 1525 km (not several thousand, as Koprowski claims) from the Ruzizi valley, and ZERO km from the other principal site in which this lot of vaccine was used (Kinshasa). The second case was in Burundi, the tiny country in which Koprowski admits the main part of his vaccine was given. The town is not specified, but no point of Burundi is over 200 km from the area of greatest vaccination. The third case was the spouse of the second case. The fourth case was about 1000 km from the site of greatest vaccination, and an equal distance from Kinshasa. However, this case was from 1975, by which time AIDS had already spread far and wide, including to Norway and the U.S. The locations of cases 5, 6, and 7 are given only as Zaire. That is all the cases this reference gives. There is not a single one that is several thousand km away from the site of Koprowski's vaccinations. The first three are extremely close. The last three are too vague to localize. For all Koprowski knows, all six of these might be zero km from a vaccination site. The only one that can be placed as much as 1000 km away did not occur until AIDS had spread far and wide. All these cases are either from Burundi or Zaire. There is no point in Zaire as much as 2000 km from the Ruzizi Valley. There is no point in Zaire that is over 1300 km from one or the other of the two main vaccination sites.
(3) That data emerging from African governments notoriously understate HIV rates is common knowledge. However, a rate of 3.7%, or 25 out of 675 random blood donors infected with a fatal infection, is extraordinarily high by any standards except the even higher infection rates to be found in Central African cities. (It is approximately 10 times the US rate, which is one of the highest in the world outside of Central Africa.) The claim that an AIDS-tainted vaccine fed (not injected) to populations would have produced much higher infection rates is not accepted by Albert Sabin, who says oral feeding of HIV-1's ancestor would have produced zero infections.[14] They need to get their stories straight. One says it cannot have happened because the rate is too high to be believed. The other says it cannot have happened because the rate is too low to be believed. There are, of course, all intermediate degrees of infection possible, from 100% down to one per million or even down to zero, depending on factors such as the concentration of contaminating virus in the vaccine and the ease with which this simian virus can establish infection in a new species when fed orally. There may have been very few who became infected. In the limit, a single infected individual could have sparked off the whole epidemic. This is, after all, the scenario of the monkey bite proponents. There is no way to decide beforehand what percentage of recipients will become infected.
One expects incidences of sexually-transmitted diseases to be much higher in urban than rural areas (this is as true in the US as in Africa), so this is a red herring. It spreads in both directions, of course. If it were started exclusively among rural populations, the chief initial spread would be from infected rural areas to the cities, where it would be rapidly amplified, and would then spread from the cities back to uninfected rural areas, and to other cities, both in the nation and around the world. The spread from rural area to rural area without going through any city in between, would be much slower. If the incidence were measured in the towns actually given vaccine, one might find a much higher incidence than in other rural areas. One cannot absolutely count on this, however, because if the number of initial infections was very low, no one in a particular town may have become infected. But one does expect to find much faster spread to the cities than from rural area to rural area, so Koprowski's "low" incidences in rural areas have very little value unless he can show that they are from a population that was vaccinated, as opposed to a rural population that was not vaccinated.
(4) Early European AIDS infections in the high incidence countries, such as France and Belgium, were not indigenous but were imported from Africa, via the strong ties these countries had there. Randy Shilts writes[24] (p. 261): "All Belgian AIDS cases at this time [March 1983], for example, were among Central Africans, largely Zairians, or people who had recently visited that continent." And on p. 392, "France reported [November 1983] the highest AIDS caseload on the continent, with 94 diagnosed patients. As in Belgium, more than half of the cases reported were natives or tourists of five African nations -- Zaire, Congo, Mali, Gabon, and Rwanda." Poland has no strong ties with Africa, nor does she have strong ties with France or Belgium or any other European country with high AIDS rates.
Koprowski correctly says that the same vaccine was given in Poland and in the suspect campaigns in Africa. He claims that the rates in Poland are too low to be consistent with that vaccine's having started AIDS. He is able to reach this conclusion only because he neglects to consider both of the two most important variables in determining the number of infections to be expected today. Those variables are the number vaccinated and the rate of spread of the virus after vaccination. Approximately 300,000 were given the vaccine in Africa. Approximately 3000 were given this allegedly contaminated batch of vaccine in Poland. The number of initial infections in Poland should have been about 1/100 of the number in Africa. But the rates of growth were certainly different also. Africa has had one of the world's fastest growth rates of HIV, and this is in large part due to the fact that it is spreading heterosexually with considerable efficiency in Africa, but with much less efficiency in Poland and other European nations. Thus the numbers infected today should differ by far more than 100-fold.
If those infected by the African virus have doubled their numbers 17 times in the 34 years since infection [counting up to 1992 when this was written], or every two years on average, it implies that the roughly 6,500,000 Central African infections were started by a mere 50 cases back in 1958. (There may have been many more initial infections, but most may have occurred to infants who died in their first few years of life without infecting anyone else.) All else being equal, 50 infections started by vaccine in Africa would imply only .5 infections in Poland, so that it may well be that no one was infected at all. This is not unrealistically low when we are talking about oral administration of a virus that is not very transmissible orally, and when we do not know whether the level of contamination was low or high.
The number of initial infections in Africa is heavily dependent on the number of doublings that have occurred, and some may find 17 doublings excessive. If instead, infections in Central Africa have doubled every 3 years on average, it implies roughly 2500 initial infections in Africa and 25 in Poland. As of April 1992, Poland was reporting 103 cases of full-blown AIDS, implying several times 103 cases of HIV infection. With the much slower growth rate in Poland, this scenario is also possible. Indeed, in a country such as Poland, where promiscuity and drug use are very low, it is perfectly possible for initial cases to decrease, if each infected person passes that infection on to less than one further person on average.
In addition to numbers vaccinated and rate of growth, there are three other factors Koprowski neglects to consider. (1) In Africa the vaccine was squirted into the children's mouths, allowing a chance for droplets to be breathed into the lungs, where any SIV particles would have been taken up by alveolar macrophages, in which they can readily multiply and cause infection. In Poland, the virus was mixed with milk and not squirted. (2) The youngest Polish vaccinees were 6 months of age, but in Africa many infants under 30 days old were vaccinated.[25] It is not without reason that newborn animals are so frequently used in attempts to transfer viruses from one species to another: their immature immune systems present much less of an obstacle to a new virus. (3) Finally, the dosages were different. Poles were given 200,000 units of the vaccine; most of the Africans also received 200,000 units, but those vaccinated in Kinshasa (then called Leopoldville) got 100,000 units, except that infants under 30 days old were given 1,500,000 units -- 7.5 times the Polish dose -- because this same immaturity of the immune system caused them to form polio antibodies less readily.[25] Giving a large extra dose to the most susceptible population, which population was not even vaccinated in Poland, might well be sufficient all by itself to account for the supposed anomaly of Poland.
There is nothing about Poland's low incidence that conflicts with the theory being put forward, and Koprowski is able to argue otherwise only by omitting or distorting all the variables necessary to do the calculation. The omissions have already been listed. He distorts by implying that the 7 million Polish vaccinees he mentioned got the same vaccine as used in Africa, when in fact only the first 3000 did so, an exaggeration of more than 2000-fold. Only 3000 had been vaccinated in Poland before Sabin informed Koprowski of the contaminating virus he had found in that particular lot of vaccine (Lot #13). When Koprowski and his associates could detect no such virus, Sabin repeated his tests and found it again.[26] This allegedly contaminated lot of vaccine was not used for the main part of the Polish campaign, which did not begin until several months after Koprowski had been informed. Nor was it used in the campaigns in Switzerland or Croatia, which Koprowski illegitimately cites as evidence that the allegedly contaminated vaccine did not start AIDS.
No one has said all of Koprowski's batches were contaminated. No one has said more than that one single batch was contaminated: the one given to 300,000 Central Africans and 3000 Poles (and no Swiss or Croatians).
[See Appendix for further details of the documentation of point (4)]
(5) Despite Koprowski's claim, the British sailor case has not been proven, nor has it even been shown to be very likely. Montagnier, Gallo, and numerous others much less renowned have contaminated their cultures with HIV-1. [Indeed, it has practically degenerated into farce, with the charges that Gallo had deliberately contaminated his cultures with the LAV sent to him by Montagnier (i.e., that he had stolen Montagnier's virus) having had to be dropped when it turned out that Montagnier's sample itself was not what he thought it was but instead had arisen when HIV from a different one of Montagnier's patients had contaminated the sample even before he had sent it to Gallo: a double contamination with a single virus first by Montagnier and then by Gallo. Gallo's opinion of who had been infected with the original virus was two steps removed from reality, and Montagnier's opinion was off by one.[27] There are many, many other horror stories detailed in What Happens When Science Goes Bad [1]] These contaminations were gross enough to grow living virus. In contrast, the PCR test, which was the only one used to confirm the British sailor's case, is so sensitive that a single DNA molecule from a single virus particle, living or dead, will often suffice to produce a positive result. Perhaps the sailor's doctors contaminated his samples while running their tests in 1990, so that the HIV they detected came from someone else (someone infected in 1990, not 1959), just as Gallo's and Montagnier's virus came from someone else.
Even if the sailor had AIDS, the example does not weigh against the thesis that Koprowski's African vaccine started HIV-1 unless the sailor was infected with HIV-1. According to D. Concar, Nature, 346: 95, 1990, the sailor's doctors have not been able to determine whether the virus they detected was HIV-1 or HIV-2. They were hoping to do so in further studies; however they have not yet published any follow-up. The HIV, incidentally, was detected in the sailor's kidney, among other places, but not in the brain, which is a favored site for HIV.
Even if the sailor did indeed have HIV-1, there are many earlier medical procedures that could have resulted in isolated cases, the earliest I am aware of being the 1916 transplant of a chimpanzee thyroid into a human being.[28] There are numerous other examples listed in the Appendix to What Happens When Science Goes Bad.[1]
[Since writing the above in 1992, I have heard talk (starting out rather hesitantly 20 months ago but by now pretty definite) that the virus was indeed HIV-1, but a modern strain of it, and thus a contaminant. A 15 September 1994 literature check still did not turn up any published reports. It does seem highly suspicious that it should take so long to characterize so important a sample as what is claimed to be the earliest case of symptomatic AIDS and the earliest infection in a person whose identity is known and whose medical records are available for study. It gains far more importance as the only counterexample yet adduced to Koprowski's vaccine as the origin of AIDS. The sailor's alleged infection was first announced in July 1990.[29] I also find it extremely disquieting that it is being sequenced by David Ho, of the Wistar Committee. At least one person who favors the polio vaccine theory has repeatedly attempted to obtain samples of the sailor's material for sequencing, and has been turned down. I have heard the thought expressed that in view of the serious implications for David Ho of the results he is getting, that their publication will be a long time coming. Perhaps the world will one day want to see to it that there are far more serious implications for David Ho if he is withholding these results.]
The 1959 Kinshasa sample was found through antibody tests, which, unlike PCR, are not subject to false positives due to minute contaminations, nor even rather gross contaminations. Such tests, of course, give false positives for other reasons. However, three different sorts of tests were carried out, and factors that might cause one test to falsely indicate a positive result would not affect the other two. Moreover, three independent laboratories tested the sample by still other means, and all these results were likewise positive.[4] Moreover, that sample fits with both the epidemiologic evidence for AIDS' origin and with one of Koprowski's vaccination sites. The AIDS establishment and I both agree that Kinshasa is a likely place to find the earliest HIV infection. The sailor's case, in contrast, is nowhere near any early center of AIDS. It does not fit with anything. And while sailors do travel, this one's travels have been very difficult to pin down (despite the Wistar Committee's undocumented claims that they have pinned them down).
(6) The sailor's AIDS-like symptoms were not manifested throughout 1958, as Koprowski asserts, but began only in December of 1958,[30] whereas a quarter million Africans had been vaccinated by April 1958, the vaccinations having begun in 1957, the first 4000 of them having been started in Stanleyville in approximately February of that year.[10] If the sailor had been in Africa and had been vaccinated, or had fallen ill, as was common among Europeans visiting Africa, and been treated with a needle previously used on an infected person (who had fallen ill for any reason, not just AIDS), he could have been infected for more than a year by the end of 1958. One year is not too early to expect the very first transfer out of Africa of a symptomatic case, in a traveler such as a sailor, a high proportion of which early cases would have attracted attention, at least if they occurred in the developed world. The sailor's doctors talked about the case with colleagues for over 20 years. (See New York Times, 24 July 1990, C3.) We forget how unusual such deaths were back then. Few would have passed unnoticed or been forgotten. There may have been only one case that made it out of Africa so early, but it is not surprising that we should have found this first case. And while one year is early to develop symptoms, it is clearly not so early as to rule this scenario out. Some people develop symptoms even more rapidly, passing into frank AIDS within a few months of first infection.[31] However, I repeat, the sailor's case has yet to be shown as due to HIV-1. [Note: the sailor suffered from gingivitis and a skin rash which his doctors say may have been eczema or tinea (ringworm) starting earlier,[30] but many, many ordinary people have such problems, and for Koprowski to claim them as proving he was already suffering from AIDS at the time these problems arose is way out of line.]
(7) The reason India's ban on export of rhesus monkeys did not affect delivery of rhesus monkeys captured in the Philippines is because there are no rhesus monkeys in the Philippines to be captured. Rhesus monkeys do not live in the Philippines.[32] A species of monkey much used in vaccine manufacture, the cynomolgus monkey, does live in the Philippines. It appears Koprowski does not know what sort of monkeys he used. Previously he told Curtis[33] that the kidneys used were bought from a supplier as monkey kidney culture material rather than as live monkeys, in which case he is forced to take the word of his supplier. Since Curtis is Koprowski's adversary, perhaps we should not accept Curtis' word either. Fortunately, Koprowski's statement in his Science letter that "even if one speculates that green monkey tissue could somehow have been mixed up with rhesus monkey tissue...." indicates he bought the kidneys already removed from the monkeys and therefore cannot attest to their identity, cannot, indeed, even say whether or not a few chimpanzee kidneys might have been mixed in. Perhaps the supplier still has records of the transaction or otherwise could surmise the species of simian, or at least narrow it down. But Koprowski has never told us the name of the supplier. Despite Koprowski's various claims to the contrary, the identity of the simians he used in the world's first oral polio vaccination campaign, which campaign is being alleged to have resulted in AIDS, quite probably to become far and away the greatest human tragedy of all time, remains a mystery.
(8) The claim that SIV-infected monkeys have no SIV in their kidneys is absurd. The claim that it has been proven is even more absurd. I thoroughly refuted the only published paper (Ohta, et al.) cited by Koprowski in support of this contention in the appendix to What Happens When Science Goes Bad,[1] well before Koprowski's letter. Lack of space prevented discussion of some of its worst errors, and its continued use by Koprowski and others prompted me to write a more complete treatment later.[18] There I pointed out eight separate fatal errors in Ohta's five-paragraph letter. Ohta himself says his cultures contained a few lymphocytes. How can some portion of these lymphocytes possibly not have been infected with SIV?
In a sworn affidavit of May 1993 given by Robert Gallo for presentation at Koprowski's libel suit against Tom Curtis and Rolling Stone (which suit was settled out of court and resulted in Rolling Stone's printing a retraction,[34] which retraction contained no mention that it was part of the settlement of a lawsuit), Gallo placed great importance on the fact that Koprowski used monolayer kidney cultures:
The Article's hypothesis that Dr. Koprowski's polio vaccine contained HIV-1, or a simian precursor to HIV-1, which infected the recipients of the vaccine in Equatorial Africa, is false. As far as we know HIV-1 does not survive in the culture of pure monkey cells. As I have been told, the Protocol for the preparation of Dr. Koprowski's polio vaccine called for the preparation of the vaccine in monolayers [his emphasis] of monkey kidney cells. CD4+ T cells and macrophages [my emphasis, see below] are the target cells for HIV-1 infection. Monolayers of monkey kidney cells do not contain CD4 lymphocytes or macrophage (sic) as far as I know. Therefore, HIV-1 should not survive in such a culture.... I do not believe that HIV-1 could have grown in monkey kidney cells used in the culture for Dr. Koprowski's polio vaccine; certainly I do not believe so learning that these were monolayer cultures.... Mr. Curtis never showed me the Protocol for the preparation of Dr. Koprowski's polio vaccine, and to my recollection never told me that the vaccine was prepared from monolayers [his emphasis].
Does not this seem a little too full of lines like "as far as I know" and "as I have been told" and "I do not believe"? Particularly does not this seem so in view of the certitude expressed in the first quoted sentence? Particularly since we are dealing here with an hypothesis about the origin of diseases through a practice that is still going on, a practice that it is alleged has certainly already started one killer immunodeficiency epidemic and quite possibly two (HIV-2), particularly since there are several other known monkey immunodeficiency viruses, both SIVs and the non-lentivirus SRVs, which latter have caused even worse epidemics in US primate colonies, plus an unknown number of undiscovered immunodeficiency viruses and other undiscovered fatal viruses that have not yet been transferred into humans but which may be transferred at any moment? (The SIVs do not cause illness in the species they are native to. They were all undiscovered until scientists accidentally transferred them into other monkey species and into humans, with results too dramatic to be missed.) One of the foremost AIDS researchers, William Haseltine of Harvard, predicts a billion HIV-1 infections by the year 2025, implying a billion deaths within less than a century of the transfer of just one of the SIVs.[35] This does not seem unreasonable: it requires 6 more doublings over the next 30 years to produce a billion infections. Yet we have learned so little from AIDS that we deliberately transplant the livers of baboons into human beings, human beings who it is hoped will survive for years or decades, thus giving whatever baboon microbes the liver may contain a familiar home (their own liver) to survive in for as long as it takes them to adapt to the unfamiliarities of human physiology, after which time they will be able to infect the rest of the patient's body, and, potentially, like HIV-1 and HIV-2, able to spread from this patient into others, infecting the rest of the body of humanity with a new human disease, perhaps to carry off its own millions or billions. And to make the baboon microbes even more comfortable in their unfamiliar new environment, to assure maximum possibility of successful transfer, the human being is to be kept deliberately immunosuppressed the whole time, just as we do with animals when we are trying to transfer a new virus into them. This is extraordinary, but it is even worse: the immunosuppressed human is then deliberately injected with baboon white blood cells, the very cells most likely to contain an SIV and which we might surmise would be most likely to contain other immunodeficiency viruses.[36]
It is more than extraordinary: it is beyond belief. Even my opponents agree that the HIVs came from simian viruses transferred into humans; the disagreement is over how the transfer occurred. If HIV-1 and HIV-2 both were transferred from monkeys through natural means, that makes it even easier, and the monkeys even more dangerous, than if natural means failed and it required the much greater intimacy of feeding unsterile monkey material to millions of human beings. The medical establishment, who thinks that I am a crackpot, should be even more adamantly against these experiments than I am. We know there are other deadly monkey viruses that have not yet transferred into our species. If a mad scientist were trying his best to transfer them, how could he possibly do any more than was done in this baboon liver transplant? AIDS' one significant weakness is that it is reasonably hard to catch, so that careful people can avoid getting it. This is not true of most diseases. What if the next plague spreads through casual contact? What if it spreads through the air? The closely-related maedi-visna lentivirus of sheep spreads through the air.[37] We could lose a lot more than a billion in lot less than 100 years. Even David Ho, perhaps the worst of the Wistar Six, said: "The baboon thing gave many of us a lot of concerns because you don't know what's in there, what possibly could be transmitted" to other people. "If the person lives, are we at risk of starting an epidemic from some primate virus or agent? That [baboon liver transplant] was done in a hurry and it's clear many things were not thought out."[38] But the starkest possible warning has already happened. We already have the clearest possible example of what an animal virus can do to our species. A member of the medical establishment calls it dangerous and foolish in a major newspaper. And yet it continues. The transplant in which the white cells were added occurred five months after this warning. If the U.S. is so reckless, then why do not other world governments object? Their people will die too. As with AIDS, they will likely die in much greater numbers than Americans (if only because there are only 1/4 billion Americans who can possibly die). But the only published objection I have seen remains that of David Ho. And the madness continues.
How did things get so out of control? Gallo's affidavit might well have been the greatest single factor persuading Rolling Stone to settle out of court and publish its retraction. Because of Rolling Stone's retraction, Science printed "Rolling Stone Rolls Over for Koprowski" and laid the matter to rest.[39] Gallo's testimony placed millions of lives at risk, yet it is transparently faulty owing to all its hedging. Why do you people let so many of your lives be risked on so flimsy a basis? Why do you stand for it? They are your lives and the lives of your children and grandchildren. The reason millions of people are dying is because you let those like Gallo and like Science get away with it (over and over again). Gallo's testimony (both the quoted part and other parts) can be shown to be false on half a dozen different grounds. Indeed, some of Gallo's own papers refute parts of it. But the best refutation was given by an anonymous referee whose response Science used as an excuse not to publish WD Hamilton's letter-to-the-editor (see above; this second rejection of 28 April 1994 came after Hamilton's strong protest letter to Science editor Daniel Koshland following the first rejection, which protest letter is reprinted at the end of this piece). That referee writes: "Anyone who has looked at a primary monkey kidney monolayer [my emphasis] culture, especially by time-lapse cinematography, will have seen numerous macrophages moving over the epithelial cells like vacuum cleaners. By secondary passage they have disappeared, but I would consider them more likely to bear HIV than the very few lymphocytes present." By "primary" cultures, it is meant that the cells were taken directly from the monkeys, and not from cell cultures that have been grown in the laboratory for many generations (or "passages"). All polio vaccine made from monkey kidney was produced in primary (first passage) cultures. Gallo's sworn statements were false. If you were not aware of them before, you are aware now. What are you going to do about it? These are not trivial matters.
(9) As to the contaminating virus Sabin claims to have found which Koprowski says was in a seed lot of virus rather than in the vaccine: what Sabin says himself is that it was used in the Belgian Congo[40] and in Poland.[41] In the former case, the quote is "tests on the large lot of Koprowski's type 1 `Chat' vaccine used in the Belgian Congo trials (Courtois et al., 1958) revealed the presence of an unidentified, non-poliomyelitis cytopathogenic virus." In the latter, the quote is: "Apparently, material having such a minimal amount of this agent diluted out in the dose that is given, has been administered without, as far as I know from what we have heard and the results in Poland and elsewhere, anything that could be attributed to it." It certainly sounds as if he is talking about vaccine, as opposed to seed lots of virus. Indeed, his second statement makes no sense if he is referring to seed lots of virus, because he speaks of the contaminating virus' minimal concentration in the material that is given. The material that is given is the vaccine itself, not the virus seed lots that are used to grow or "seed" the vaccine, in the same way yogurt culture is used to seed each new batch of yogurt. Just as a small addition of a few yogurt culture cells or a little seed virus can increase enormously within a few days in making the final product, a small concentration of a contaminant in a seed virus could grow into a very heavy concentration in the finished vaccine. If what Sabin tested was the seed lot, he would have no basis for his statement that the vaccine itself contained a minimal amount. This is a trivial point, and Sabin was certainly aware of it. Joseph Melnick also says, "A simian virus has been reported as a contaminant of at least one batch of vaccine that has been used in the Belgian Congo and elsewhere."[42] And Koprowski's own colleague Sven Gard of Sweden, who is one of the two besides Koprowski who tested and failed to find the contaminant, states: "I would like to make some remarks with regard to Dr. Melnick's and Dr. Sabin's comments on the presence of extraneous viruses in the vaccine used in the Belgian Congo. We have used exactly the same lot for our experiments in Sweden...."[43] It is clear these references are to lots of vaccine and not to seed lots. Koprowski himself was present at the conference in which Sabin, Melnick, and Gard made their comments, yet he made no effort to correct their statements. Indeed, Koprowski himself writes (in a reference he himself cites in his Science letter): "Sabin states that tests of the Chat strain in his laboratory revealed the presence of `an unidentified, non-poliomyelitis cytopathogenic virus' in the pool" (my emphasis). Two sentences later Koprowski writes, "Two laboratories, apart from our own, have performed identity tests on the large Chat pool mentioned by Sabin..." (my emphasis).[44] It seems unmistakably clear that it was a pool of vaccine and not a seed lot that was being referred to. If this is not the case, then we are dealing with a very subtle and confusing concept which I am still failing to grasp, and which many readers will likewise fail to grasp, and perhaps Dr. Koprowski would like to explain in clearer terms what he meant in his letter to Science and what he meant in his letter to British Medical Journal and what Sabin meant in British Medical Journal and what Sabin and Melnick and his own colleague Gard meant in the First International Conference on Live Poliovirus Vaccines. Koprowski mentions that he and two other laboratories were unable to find this virus, but he neglects to mention that in view of this failure Sabin repeated his tests and detected the virus a second time.[45] Is this how scientists handle conflicting data: cite that which supports you and pretend the rest do not exist (and hope that nobody notices)? Sabin was one of the most careful experimentalists of his generation, and far more eminent than Koprowski. His claim of contamination is not to be dismissed so lightly. Please Dr. Koprowski or Dr. Sabin, provide us with a sample of this allegedly contaminated material so that we can test it now. We have a vaccine claimed by the father of all current live polio vaccine to be contaminated, which vaccine was given under questionable circumstances to colonial subjects of another country several years before any such vaccine was licensed for use in the U.S. -- indeed this was the first such mass vaccination campaign in the world -- which contaminating virus no one ever bothered to identify, and all samples of this historic and called-into-question vaccine now mysteriously appear to be missing. Can no one see that this is outrageously inexcusable behavior even if this vaccine did not start AIDS? [This plea for Koprowski or Sabin to provide samples was written in 1992; Sabin died 3 March 1993.]
(10) Once again, the claim is that a single batch of vaccine was contaminated. This batch was not used at all in Switzerland or Croatia, and only 3000 doses were given in Poland. (See Appendix for more details.)
(11) It was Curtis' impression (as my own also) that vaccine, in addition to seed lots of virus, was stored at the Wistar Institute; but if this is incorrect it is very important to have found it out. It is crucial to test the vaccine itself and not just the seed lots. The vaccine would have been made by adding the seed lot to monkey kidneys. If the SIV was in these monkey kidneys, then testing the seed lot would erroneously give a negative result. If vaccine samples are not stored at Wistar, then where are they stored? This is one of the few points Koprowski may have scored against Curtis. Readers can judge for themselves whether it makes any difference at all.
(12) Koprowski simply fails to understand what this whole matter is all about. The claim is that a small proportion (probably under 1%) of those receiving a single batch of Koprowski's vaccine became infected with an SIV that was contaminating it, and these few infected people infected others, who infected others, to form the current worldwide epidemic of AIDS. There has been no follow up that would have detected illnesses occurring years after vaccination in a very small proportion of vaccinees in Central Africa.
Koprowski made only one correct claim against Curtis of slight importance (the HIV incidence in Katana has been scaled back, but there is plenty of other evidence for the high rates nearby), and one probably correct claim of no importance (vaccinations not in Kivu district but across the river), and one claim which does not affect the case in any way (only seed lots stored at Wistar). He had a very long piece in a non-science journal to work with. In contrast, in his two-page letter in a respected professional journal, I was able to find 9 provable errors, 6 of them serious. [The 6 serious ones being "Completely wrong"; several thousand km away; no mention of 3000 vaccinations or slower growth rate in Poland while implying 7,000,000 vaccinations and no mention of younger children given higher dosages in Africa and no mention that the suspect batch was not even used in Switzerland or Croatia -- someone less generous might have counted this as two or three or four or five or six or seven errors; does not know what monkeys he used; SIV doesn't exist in monkey kidneys; follow-up has shown vaccine to be safe.]
In addition to these errors found by me, Tom Curtis was the first to note that the reference Koprowski cites as evidence that he used rhesus monkeys for his vaccine says no such thing. He is also responsible for the information, mentioned above, that the Polish vaccine was not squirted. These were in his rebuttal, which Science refused to publish.
A person who writes on an important subject (it is surely important to Koprowski: he is accused of being the father of AIDS) and gets every single significant point wrong is either grotesquely incompetent (if he is doing his best) or a deliberate liar (if his errors are calculated). A publication that prints these errors on a matter of the greatest historic importance is incompetent (when even a spot check could not have failed to detect the problems) or is a willing participant in the deception. When that publication then refuses to correct the errors it disseminated even when they are pointed out by one of the most eminent biologists of our day, this is not incompetence but clear corruption. If you put grotesquely incompetent and corrupt people in charge of matters where hundreds of millions of lives are precariously hanging in the balance, the probable result is all too predictable. WD Hamilton wrote in his first letter to me (30 December 1991): "Your scenario accords with everything I believe likely about the origin of new diseases and about the evolutionary sequence such interspecies invasions are likely to go through.... I must say that had I known, as I easily could have found out, as you did, that they were injecting or making me eat raw extracts of the tissues of a primate with nothing done to eliminate or incapacitate other viruses I would have immediately refused the inoculations" (emphases his). Hamilton, one of the most eminent evolutionists of this century, had he known what they were doing, could have told them that it was highly dangerous and might well result in the transfer of new diseases. Had he done so in 1957 (which, however, was before he had become prominent) and had they listened, perhaps a billion lives might have been saved in just the next century. Well he knows now. And he has told them now. And the evidence for AIDS' origin is enough to make any sane person listen now. How many future AIDS epidemics will we avoid if the warnings are heeded, if the lessons are learned? How many future catastrophes await us if we prove unteachable?
The reason we know the African vaccine was also used in Poland on 3000 people is because in several places the Polish vaccine is given as Lot 13, the lot of the African vaccine (see below; see also note 25 of my What Happens When Science Goes Bad[1] for the lot number of the African vaccine), while the number vaccinated is given as 2888 in the town of Wyszkow and the neighboring villages plus 22 in Warsaw plus 32 separately vaccinated in a boys' school (which may have already been counted among the 2888; I couldn't tell). These figures are from pp. 498-9 of Przesmycki P, Dobrowolska H, Olakowski T, Stanczyk R, Naruszewicz D, Report on Field Trials with Live Attenuated Poliomyelitis Vaccine in Poland, First International Conference on Live Poliovirus Vaccines, Pan American Sanitary Bureau (Pan American Health Organization Scientific Publication No. 44), Washington, D.C., 1959, 497-507. The lot number (13) is given in Table 1, p. 497. The dosage (200,000 units) and the age of the youngest vaccinees (6 months), are given on p. 498. In the Discussion which followed, p. 508, Koprowski says the same pool of vaccine was used in Leopoldville (today called Kinshasa) as in this Polish vaccine. Moreover, this is confirmed by several specific mentions of Lot 13 as the Leopoldville vaccine, such as on p. 416 of the same First International Conference. Both the Polish lot number and the number vaccinated are also given in Przesmycki F, Dobrowolska H, Georgiades J, Olakowski T, Stanczyk R, Naruszewicz D, American Journal of Hygiene, 71: 275-84, 1960. This small 3000-person trial was begun 20 October 1958, the date being given in Przesmycki F, Dobrowolska H, Mirski B, Stanczyk R, Wior H, Zaleska H, Bulletin of the World Health Organization, 26: 733-43, 1962.
On p. 733 of this latter article, we read: "On the basis of an analysis of these results, a special committee appointed in 1959... ordered that mass vaccinations... be organized throughout Poland, according to the following plan:
(1) Children... 6 months to 7 years... (2) Children 7 years or older..."
In other words, children under 6 months of age were not vaccinated in Poland.
A little later in this article, we see: "Throughout the entire vaccination period, a single pool of type 1 vaccine and a single pool of type 3 vaccine, obtained in several batches, were used."
This is referring to the large 7,000,000-person vaccination campaign, and not the 3000-person pilot campaign of the year before. The article does not give the number of the single pool used, but it can be shown through at least two means that the claim that all vaccine came from the same pool did not apply to the small 3000-person trial of the year before. First of all, at least by 14 March 1959, when Sabin wrote about it in British Medical Journal, p. 678, Koprowski had been informed by Sabin that the vaccine he had used for the 3000-person campaign was contaminated; and the larger campaign in Poland did not begin until June 1959. It is inconceivable that Koprowski would have gone ahead and used this allegedly contaminated vaccine anyway, or that the Polish authorities would have permitted him to go ahead if he had been foolish enough to want to. Even if he were absolutely convinced Sabin was mistaken, he would still be putting himself in an impossible position because parents of children who fell ill afterwards could sue him claiming that it was his contaminated vaccine that did it, and he could not defend himself if he had to admit to knowingly giving out vaccine that a prominent researcher had said was contaminated. Not even Koprowski would have been that reckless (and let him dispute that fact if he wants to).
The second reason we know the large Polish campaign did not use Lot 13 comes in another paper on this campaign. This paper is from the Second International Conference on Live Poliovirus Vaccines, Pan American Health Organization (Scientific Publication No. 50), Washington, DC, 1960, pp. 522-30, and is by Przesmycki F, Dobrowolska H, Mirski B, Stanczyk R, Wior H, and Zaleska A. This gives (pp. 522-23) two batch numbers, Wistar CHAT 18 and Wistar CHAT 18 GH, which I presume together made up Pool 18, which would have been the single pool used for the major part of the campaign. [Note that "batch," "lot," and "pool," have somewhat fluid meanings. They are sometimes used interchangeably. Melnick in First International Conference on Live Poliovirus Vaccines, p. 577 calls the contaminated vaccine a batch; on p. 579 Gard calls the same "batch" a lot; in British Medical Journal, 14 March 1959, 678, Sabin also calls it a lot; and in the same source 23 May 1959, 1349, Koprowski describes it as a pool. Often, however, there is a distinction drawn between pool and batch, with pools consisting of several batches mixed together. I have never seen a precise definition of these terms.]
This same paper, incidentally, p. 525, also mentions that 13 children were mistakenly injected with vaccine by a nurse. If this had been the contaminated batch, we might have had 13 infections right there. Such accidents will inevitably happen, and people who say oral vaccine is safe because HIV cannot be passed orally would be badly wrong for this reason even if they were not already badly wrong about oral transmission (and even if they were not badly wrong about completely unknown viruses). Once the infection is established in a single person, the entire race is at grave risk if this patient ever passes the infection on.
The June 1959 date for the beginning of the major part of the Polish campaign (i.e., the first vaccinations after the 3000-person trial of 1958) is repeated in this paper, on p. 525. This larger campaign also included only children over 6 months of age (p. 522). On p. 526 the dosage is given as 200,000 units.
So the allegedly contaminated African vaccine, Lot 13, would not have been used anywhere after Sabin announced his finding of contamination in March 1959, and this is how we know the later Swiss and Croatian campaigns did not use this lot. In Plotkin SA, American Journal of Public Health, 52: 946-60, 1962, the first sentence reads: "In 1959 through 1961 the CHAT Type 1 and W-Fox Type 3 attenuated poliovirus strains of Koprowski were administered on a mass scale to Polish, Croatian, and Swiss children." On p. 959 it gives the specifics of the Swiss campaign. "In 1960, 40,000 children in Aargau and Basel were given CHAT, and in the first half of 1961, 320,000 children in the cantons of Bern, Luzern, and Aargau were given both CHAT and W-Fox." On p. 958-59 it gives the dates of the campaign in the Croatian Republic of Yugoslavia as 18 February - 4 March 1961, during which 1,340,000 got CHAT vaccine. They do not give the lot numbers, but all this is well after they would have had to stop using the African vaccine because of Sabin's claim of contamination.
The following discussion makes the assumption that HIV-1, both the old variety and now this new one, came originally from chimpanzees. This is in my view much the most likely possibility, though there are also more complicated sets of circumstances that can explain all the facts, such as a second, rarer SIV existing in African green monkeys, which in addition to being rare and undiscovered (except perhaps by Lecatsas and Alexander[9]) is very closely, and recently, related to the chimpanzee SIV. Perhaps green monkeys infected chimpanzees in recent times, or vice versa. We shall ignore this possibility in what follows.
If Koprowski's contamination was already present in the kidneys from his unnamed commercial supplier at the time they were purchased, especially if it occurred as a result of chimpanzee kidneys being mixed in, there is the potential for some other vaccination campaign using this supplier to have started a divergent strain of HIV-1. It could also have come about through a separate batch of Koprowski's vaccine given shortly after the campaigns that transferred the original HIV-1[46] and perhaps made from simians from the same supplier, or otherwise subject to whatever factors caused the first contamination. And there are other possibilities as well, mainly owing to the great number of vaccine batches that have been manufactured in the latter half of this century, made in many countries and using techniques of varying sophistication, which would be expected from time to time to allow contamination from a virus existing in one of the chimpanzees used in medical research, and specifically in vaccine research. How often this would happen is unclear, but certainly neither once nor twice in over thirty years is implausible.
The aberrant HIV-1 strain was originally isolated in a couple from Cameroon who had moved to Belgium.[47] This virus is noteworthy because it traces its ancestry with the common HIV-1 to an even earlier period than the single chimpanzee virus that has been used for comparison purposes.[48] This has caused considerable confusion among researchers studying the new virus, but it makes perfect sense if it was due to a second batch of vaccine containing virus from a different chimpanzee individual. I will spend several paragraphs going over the confusing point carefully enough that anyone who will take a few moments to think it over, and who will draw a couple of diagrams of the sort that are puzzling the researchers, will be able to understand.
First, it is important to ascertain that this is a real virus and not an artifact caused by still further contamination. Thus, there was a notorious case of multiple contaminations of Kanki's and Essex's samples which they had taken from African green monkeys and from Senegalese prostitutes. They contaminated these samples with a macaque SIV that they were studying at the same time and wrote an important paper announcing the discovery of African green monkey SIV, which later turned out to be the contaminating macaque SIV instead (though African green monkeys do indeed have their own legitimate SIV as well). Several of the Belgian researchers who reported the new, aberrant HIV-1 strain were the same researchers who had been studying chimpanzee SIVs. My first thought was that this was no coincidence and that a chimpanzee virus had contaminated their Cameroonian cultures.
However, the new virus very strongly appears to be real. A separate group of researchers, unknown to the first, has isolated another example of this aberrant virus, also in a patient from Cameroon.[49] And both groups have tested HIV-infected Cameroonians and found that 5-10 percent of Cameroonian HIV-1 cases appear to be due to this new virus. This would represent several thousand total cases, yet only a handful of cases have been detected anywhere in the world outside of Cameroon and the bordering country of Gabon.[50]
So the parts of this paper which say there has been only one introduction of HIV-1 now very strongly look as if they need to be changed. The heavily localized nature of this new virus almost certainly indicates a recent introduction, perhaps significantly more recent than the 1957-8 introduction of the original HIV-1. A third appearance of a simian immunodeficiency virus in human beings around the middle part of this century, or later, which like HIV-2 and the earlier form of HIV-1 also seems to have sprung up out of nowhere, if such these new cases be, would represent still more very powerful evidence for a vaccinal origin.
But while these new cases might be a good thing for my theory of AIDS' origin, a new strain of HIV-1 would represent a very bad thing for the world. I would be willing to trade many millions of extra cases of the old HIV-1, more millions of cases than now exist in the world, for a handful of cases representing a new introduction of HIV-1 from a different chimpanzee individual. If the goal is the minimization of resulting deaths, my guess is that while I would come out far behind in the short run, I would end up well ahead in the long run. The final excess toll from this new introduction, compared to what would have happened without it, is likely to be far greater than the 20 million or so HIV-1 cases that now exist in the world.[51]
To turn now to the point that is puzzling researchers: If the genetic sequence of this new virus is compared with the sequences of other HIV-1 strains, and a phylogenetic "family tree" is drawn indicating the relationships among these strains, it is seen that the new strain does not have any common ancestor with the previous strains (all of which have common ancestors with each other around 1958 or later) until a very long time ago (see papers cited in notes 48 and 49). Indeed, even the single chimpanzee virus that has been used for comparison purposes joins this family tree more recently than the new HIV-1 virus. The chimpanzee virus joins the family tree perhaps 150 or more years ago. The new HIV-1 virus joins significantly earlier than that.
Well if the virus was in humans earlier than it was in chimpanzees, it looks as if it was humans that infected chimpanzees and not the other way around. One group not only made this suggestion but said moreover that because a similar situation obtains with sooty mangabeys and an aberrant HIV-2 virus, it looks as if sooty mangabeys and chimpanzees both acquired their infections long ago, perhaps centuries or millennia ago, from human beings.[52]
But there are several errors in this line of thought. The most obvious is one I mentioned earlier, in the Background section at the beginning of this paper and in note 11: Why do they decide that the ancestor virus of some hundreds of years ago existed in a human being rather than a chimpanzee? A chimpanzee virus of a few hundred years ago could by now have given rise to a diverse family of viruses, just as the human virus has greatly diversified in less than four decades. If during the middle or latter part of this century you transfer two of these now-diversified chimpanzee viruses into humans through two different vaccines, then all the mysteries are explained. Otherwise, you have all kinds of anomalies and weirdnesses, such as implausible long-ago transfers from humans into chimpanzees and sooty mangabeys of two different viruses, when all evidence indicates neither one of these viruses existed in human beings until very recently. And then there is the question of all the missing branches of the family tree. I gave that argument also in note 11. Although this anomalous HIV-1 subtype complicates the analysis, and I will not go into the new version here, the existence of this new HIV-1 greatly strengthens that argument. At least this is so if comparisons of various cases of this new HIV-1 shows them all to have a common ancestor (with each other) sometime after the middle part of this century. I have little doubt that this is what the phylogenetic tree will reveal. The two cases of this new virus that have so far been sequenced have a common ancestor that at first glance looks to be almost exactly as recent as the time of transfer of the earlier HIV-1.[53] Because of the very localized nature of the new virus, I would have expected the transfer to be significantly more recent than that of the original HIV-1, but there are several simple ways of reconciling the dates with the epidemiology.[54]
There is a second error that led these researchers to make their preposterous suggestion that human beings had been infected all along and were the ones passing the viruses to simians and not the other way around. They are using the sequence of one single chimpanzee virus (and one mangabey virus) to do their comparisons. They have made the assumption that this is "the" chimpanzee virus.
But why would a virus that varies so rapidly in human beings and which comes in such widely divergent forms, exist in only one form in chimpanzees? (Within the few decades in which the original type of HIV-1 has been in humans, differences up to about 30 percent in nucleotide sequence of the envelope part of the virus have already emerged.[48]) If chimpanzees have been infected for a long time, then presumably these chimpanzee viruses have diverged over the years to form a very variable family of viruses. Indeed this is just what we find when we look at the SIV of African green monkeys. This virus has been examined through sequencing samples from a number of monkeys, and when the phylogenetic tree for green monkey SIV is drawn, we see that that virus has diversified far more than has HIV-1.[55] The reason "the" chimpanzee virus joins the family tree more recently than the aberrant HIV-1 virus is that we are examining the family tree of three different chimpanzee viruses. We are picking one of them, namely the chimpanzee virus that found its way into Koprowski's vaccine in 1957, and comparing it with each of the other two in turn. If chimpanzees are like humans and like green monkeys in having a highly diversified family of these viruses, then one of these two might differ significantly from the other in the date at which it had a common ancestor with the Koprowski virus. (Indeed, this would be true even if all chimpanzee virus samples were identical down to the last nucleotide, only in that case sequence analysis could not be used to determine the family tree.) It turns out that the chimpanzee virus that has been sequenced and is being thought of by researchers as "the" chimpanzee virus, has a common ancestor with the Koprowski vaccine chimpanzee virus significantly more recently than the chimpanzee virus that has now found its way into human beings in Cameroon. It could as easily have been the other way around.
Depending on which two of the large SIV family existing in chimpanzees we pick to compare against each other, we will get widely differing dates for their most recent common ancestor. This date might go back as early as the first introduction of these viruses into chimpanzees and would certainly in any case be as recent as the date at which the last chimpanzee infected any other chimpanzee (i.e., presumably this year), if those two chimpanzees were the ones whose viruses were compared.
If this is confusing, it will be extremely helpful to draw a picture: Assume chimpanzee 1a is the first to be infected with the ancestral SIV, perhaps some hundreds of years ago. Chimpanzee 1a infects chimpanzees 2b and 2c. Chimpanzee 2b infects 3d and 3e. Chimpanzee 2c infects 3f, 3g, and 3h. Now if we look for the most recent common ancestor of 3f and 3g, we see that it was the virus in chimpanzee 2c. But if we look for the most recent common ancestor of some other "third generation" cases, such as 3f and 3e, we see that we have to go back to 1a. And all the descendant viruses of 3f, 10,000 years later, when compared against any of the descendant viruses of 3e, 10,000 years later, will again be forced to go all the way back to 1a before the first ancestor of both viruses is encountered. Yet there will also be cases 10,000 years later that only have to go back one single step before encountering the ancestor virus in the chimpanzee that infected them both, just as in the cases of 3f and 3g, above. Depending on which two viruses we compare against each other 10,000 years hence, we could get values ranging from a few years to 10,000 years, or anywhere in between.
So there is nothing puzzling about finding a chimpanzee virus whose ancestor with the human virus is more remote than the chimpanzee virus previously sequenced. And if that more-remote chimpanzee virus was passed on to human beings in Cameroon, that human isolate would be more remote from the rest of HIV-1 than is the earlier sequenced chimpanzee virus.
Extend the picture you have just drawn: Assume the virus from chimpanzee 3e contaminates a batch of vaccine. Assume the virus from 3f contaminates a second batch of vaccine. Assume the first batch is given in 1958 and the second in 1980. Assume chimpanzee 3d is the chimpanzee whose virus is sequenced and is being presumed to be "the" chimpanzee virus. Then the phylogenetic tree of the two human viruses and "the" chimpanzee virus will show the second (1980) human virus to have a common ancestor with the first at the time of chimpanzee 1a. "The" chimpanzee virus, however, will have a common ancestor with the original, 1958 vaccine virus as recently as chimpanzee 2b. This is the same situation as now exists with the actual viruses that have been sequenced and compared. The conclusion is being drawn that the Cameroonian virus is "more remote" than "the" chimpanzee virus. If they will just sequence a few more viruses from chimpanzees, they will see that some are more remote than the Cameroonian virus and some less remote.[56] In the above diagram, comparing virus from chimpanzee 3g instead of 3d would exactly reverse the situation. Had the human viruses come from chimpanzees 3d and 3e, and had "the" chimpanzee virus come from 3f, "the" chimpanzee virus would now be more remote than either human virus.
Look at the diagram depicting the actual family tree of African green monkey SIV in the paper by Johnson, et al., discussed above[55] (or, rather, that portion of the tree represented by the relatively few viruses they have so far sequenced and compared). Try the thought experiment of transferring two of these viruses into humans through vaccines and then comparing them with a third. See what a dramatic difference it makes depending on which three you pick. Choose, say, SIVagm90 for the 1958 vaccine batch, SIVgri-1 for the 1980 batch, and SIVtyo-1 for "the" virus in green monkeys. Then try SIVver-1 as "the" green monkey virus instead. The picture will be hopelessly confusing, so long as one does not realize we are dealing with multiple recent transfers into humans from members of a very diverse virus family which traces its lineage back for probably hundreds of years in any given species it naturally infects.
It now very strongly appears there was a second, independent introduction of HIV-1. Assuming it arose through a second batch of contaminated vaccine which had introduced another single strain of virus, then all such cases, when compared against one another, should have common ancestors around or after the middle part of this century (i.e., around or after the date of introduction), and all such cases, when compared against standard HIV-1 cases should have common ancestors 150 or more years ago when the two chimpanzee viruses that contaminated the two vaccines had their own common ancestor in chimpanzees.
Although the single diagram I have seen of the first two discovered cases of this new virus make its introduction look to be almost simultaneous with the Koprowski introduction, possibilities for significant errors arising from just two cases, and from dramatically speeded up evolution immediately following introduction into a new species, make the conclusion of near-simultaneous transfer questionable (see note 11). In particular, the extremely localized nature of the new virus immediately makes one suspect a significantly more recent introduction, perhaps 10-20 years after the first (in which case it could not have come from one of Koprowski's vaccines). I would start out looking at vaccination campaigns waged between about 1965-85 as the best bets, while recognizing that earlier campaigns are also a definite possibility.[57]
If this is a quite recent transfer, it is likely that some or many of the current cases were infected directly by the (presumed) vaccine, and not from other infected humans. Assuming there was only one contaminating strain in the vaccine, then each one of these first victims received (virtually) identical viruses. Since the virus has been diverging within the body of each person from the time the infection was acquired, one cannot expect to get perfect matches by comparing viruses from two such people some years later. But the matches would still be significantly closer than should otherwise be expected. And it may be possible to find blood samples, taken just shortly after the vaccine was given, that show identical viruses in disparate people and thereby prove unequivocally that the infection was not a natural occurrence.
[This document is copyright (C) 1995 by Louis Pascal. However, please feel free to make and distribute copies of this document, or of my companion piece pointing out errors in Ohta et al., or of What Happens When Science Goes Bad. But no parts are to be altered or omitted.]
[2] Gillon R. A startling 19,000-word thesis on the origin of AIDS: should the JME have published it? Journal of Medical Ethics, 18: 3-4, 1992.
[3] Koprowski H. AIDS and the polio vaccine. Science, 257: 1024-7, 21 August 1992.
[4] Nahmias AJ, Weiss J, Yao X, et al. Evidence for human infection with an HTLV-III/LAV-like virus in central Africa, 1959. Lancet, 1: 1279-1280, 31 May 1986. The alleged HIV infection of a British sailor, based on autopsy material taken in 1959, is very much contested. See the response to point 5, in the text.
[5] Geissler E, Scherneck S, Waehlte H, et al. Further studies on the relationship of SV40-like viruses to human tumors. In: Essex M, Todaro G, zur Hausen H, eds. Viruses in Naturally Occurring Cancers. Cold Spring Harbor, New York: Cold Spring Harbor Laboratory, 1980: 343-355. See also p. 1026 of Koprowski's letter to Science (Ref. 3), where he admits also to contamination with foamy virus, a simian retrovirus currently believed to be harmless.
[6] Koprowski H. The tin anniversary of the development of live poliovirus vaccine. In: Second International Conference on Live Poliovirus Vaccines. Washington, DC: Pan American Health Organization, 1960: 5-11. (Pan American Health Organization Scientific Publication No. 50.) See p. 7.
[7] a. Sabin AB. Present position of immunization against poliomyelitis with live virus vaccines. British Medical Journal, 1: 663-680, 14 March 1959. b. Sabin AB. Discussion. In: First International Conference on Live Poliovirus Vaccines. Washington, DC: Pan American Sanitary Bureau, 1959 (Pan American Health Organization Scientific Publication No. 44), 577-579.
[8] Levy JA. Pathogenesis of human immunodeficiency virus infection. Microbiological Reviews, 57: 183-289, 1993.
[9] Lecatsas G, Alexander JJ. Origins of HIV (letter). Lancet, 339: 1427, 6 June 1992. See also Curtis Tom. Monkey may offer `missing link' to induction of AIDS virus. Houston Post, 2 August 1992, A1.
[10] Courtois G, Flack A, Jervis GA, Koprowski H, Ninane G. Preliminary report on mass vaccination of man with live attenuated poliomyelitis virus in the Belgian Congo and Ruanda-Urundi. British Medical Journal, 2: 187-190, 26 July 1958. Samples from 2 pools of vaccine, one for type 1 polio and one for type 3, were tested on 5 chimpanzees each; see p. 188.
[11] a. Sharp PM, Li W-H. Understanding the origins of AIDS viruses. Nature, 336: 315, 24 November 1988. b. Li W-H, Tanimura M, Sharp PM. Rates and dates of divergence between AIDS virus nucleotide sequences. Molecular Biology and Evolution, 5: 313-330, July 1988. (See especially Table 5.) Several groups have employed backward projection of divergence to estimate the date of AIDS' origin. Every one I have seen is compatible with my own date. This group came closest, but that is not the only reason I have cited them. By considering only changes to nucleotides that do not result in changes to amino acid sequence, and are therefore nearly neutral with respect to selection, they avoid two large sources of error. I do not know of any other study that avoided these errors. (However, I have not looked for such studies lately.)
The alternative dates some have put forward of hundreds or thousands of years ago are uniformly arrived at by positing the date at which HIV-1 and HIV-2 had a common ancestor. The assumption is made that this common ancestor was in human beings, rather than in simians. (Thus they say it would have taken hundreds of years for the large differences between HIV-1 and HIV-2 to evolve.) There is no basis whatever for the assumption that the common ancestor was in humans. There is considerable evidence against it, since HIV-2 also traces its origin point in human beings back to roughly the same 1950s or 1960s date as HIV-1, and there is no trace anywhere of the human cases that would have had to exist for the hundreds or thousands of years when HIV-1 and HIV-2 were evolving from their common ancestor, if the evolution took place in human beings. The evidence would be available in the descendant cases they had left: when we compared the sequences of two such descendants whose common ancestor lived in 1900 or 1850, we would get the dates 1900 or 1850 (approximately); yet there are no such cases. No matter which two isolates we compare against one another, the earliest date remains roughly 1958. [But see Addendum.] Both HIV-1 and HIV-2 appear to have sprung up out of nowhere in the middle part of this century. It is far more likely that the evolution was in simians, not humans, and the two viruses were transmitted ready-made into humans through two different transfers both occurring around the middle part of this century. In my scenario, these transfers would have occurred through two separate vaccine accidents, involving, in all likelihood, two different species of simians. In any event, since the date of hundreds of years ago entirely depends on the assumption that my explanation of two separate recent transfers is false, it cannot be used as evidence against that explanation, as has been attempted in correspondence sent to Brian Martin by R.M. May. His date is arrived at by assuming my explanation is false, which date is then cited as evidence that I am wrong. It is an elementary case of assuming what is to be proved. If I am wrong and there was one non-vaccinal transfer, then the procedure gives a date of hundreds of years ago (while leaving a large, unsatisfying puzzle, with all pieces before the 1950s unaccountably missing). If I am right and there were two transfers via vaccine, then the procedure gives a date of roughly 1958, which accords perfectly with the date of Koprowski's vaccination campaign (and the reason the puzzle pieces are missing is that there truly were no human cases before the middle part of this century). Indeed, the one paper cited by May in his correspondence with Martin (Eigen M, Nieselt-Struwe K. How old is the immunodeficiency virus? AIDS, 4(supplement 1): S85-S93, 1990, also known as AIDS 1990: A Year in Review), says itself two different times that their conclusion is not for a one-time transfer hundreds of years ago when HIV-1 and -2 had a common ancestor, but that the transfer may have occurred twice far more recently.
My claim is not that there was one transfer via vaccine which then evolved into HIV-1 and HIV-2. That is a foolish claim which can indeed be shown to be false through these means (and others). My claim is that in the middle part of this century two different transfers from two different simians occurred, one clearly through a vaccine, while the other has not been firmly pinned down but there is every reason to believe it also occurred through a vaccine or some other medical procedure involving simians. What do you get when you apply these dating methods not to a straw-man theory but to the one I have put forward? Is there a single research group that has produced a result that is incompatible? One would like to accuse May of deliberate deception (and there is some evidence of this), but if he did not bother even to read the paper he cited as disproving my views, there is no reason to believe he bothered to read my paper either. [And if my reaction seems unduly hostile, perhaps it can be better understood if I quote from his letter of 12 February 1992: "What I find irritating is that this line of evidence is simply ignored by Pascal, who writes more as if he were on a soap-box in Hyde Park than as if he were offering something to a scholarly journal. This is not simply a matter of the establishment wanting things in canonical form. But rather is a matter of respect for evidence." This letter, to Brian Martin, whom he had once been PhD advisor for, neglected to mention anywhere in it that May and I have been bitter enemies since 1988, and that I do not know of anyone who has played a larger role in blocking either my ideas about AIDS' origin or my even earlier ideas claiming that both AIDS' virulence and its transmissibility would increase in the future as it became better able to grow in its new environments, the human body and the human race, ideas based on elementary theoretical arguments for which experimental evidence is now beginning to appear (see Ref. 8, pp. 221-2, 241; also see Anonymous. AIDS: the third wave. Lancet, 343: 186-8, 22 January 1994). These are two of the most important ideas about AIDS that there could possibly be: where it came from (and where other such plagues will likely come from if we keep it up) and where it is going. Both were entirely missed by the establishment. More than missed: they were blocked --for 6-1/2 and 8 years years, respectively, and counting.]
[12] Bohannon RC, Donehower LA, Ford RJ. Isolation of a Type D Retrovirus from B-Cell Lymphomas of a Patient with AIDS. Journal of Virology, 65: 5663-72, November 1991.
[13] Curtis T. `Easy test' for theory on AIDS. Houston Post, 16 March 1992, A1.
[14] Curtis T. Do cold, hard AIDS facts lie in freezer? Houston Post, 8 May 1992, A1.
[15] Van de Perre P, Simonon A, Msellati P, et al. Postnatal transmission of human immunodeficiency virus type 1 from mother to infant. New England Journal of Medicine, 325: 593-8, 29 August 1991.
[16] Basilico C, Buck C, Desrosiers R, Ho D, Lilly F, Wimmer E. Report from the AIDS/Polio-virus Advisory Committee. Wistar Institute of Anatomy and Biology, 3601 Spruce St., Philadelphia, PA 19104, 18 September 1992.
[17] Ohta Y, Tsujimoto H, Ishikawa K, et al. No evidence for the contamination of live oral poliomyelitis vaccines with simian immunodeficiency virus. AIDS, 3: 183-184, March 1989.
[18] Pascal L. Preliminary Notes Concerning Shortcomings of a Correspondence by Y. Ohta, et al., Entitled "No Evidence for the Contamination of Live Oral Poliomyelitis Vaccines with Simian Immunodeficiency Virus," Published in AIDS, 3: 183-4, 1989. Unpublished. 8 May 1993.
[19] Curtis T. Scientists urge major changes in how polio vaccines made. Houston Post, 23 October 1992, A16.
[20] Hamilton WD, letter to Louis Pascal, 16 September 1993.
[21] Curtis T. The origin of AIDS. Rolling Stone, 19 March 1992, 54-60, 106-8.
[22] Science, 257: 1463, 11 September 1992.
[23] The 6.5% figure was obtained by tracing the map on a sheet of graph paper and counting the squares.
[24] Shilts R. And the Band Played On. New York: St. Martin's Press, 1987.
[25] Lebrun A, Cerf J, Gelfand HM, Courtois G, Plotkin SA, Koprowski H. Vaccination with the CHAT strain of type 1 attenuated poliomyelitis virus in Leopoldville, Belgian Congo. Bulletin of the World Health Organization, 22: 203-213, 1960. See p. 204; also see note 15 of Ref. 1.
[26] See Ref. 7b, p. 579.
[27] Culliton BJ. Contaminated origin of AIDS viruses. Nature, 351: 267, 23 May 1991. See also Wain-Hobson S, Myers G. Too close for comfort. Nature, 347: 18, 6 September 1990, for a possible 4-level HIV contamination.
[28] Voronoff S. Life: A Study of the Means of Restoring Vital Energy and Prolonging Life. EP Dutton, 1920, 106.
[29] Corbitt G, Bailey AS, Williams G. HIV infection in Manchester, 1959. Lancet, 336: 51, 7 July 1990.
[30] Williams G, Stretton TB, Leonard JC. Cytomegalic inclusion disease and Pneumocystis carinii infection in an adult. Lancet, 2: 951-5, 29 October 1960.
[31] Pedersen C, Nielsen JO, Dickmeis E, Jordal L. Early progression to AIDS following primary HIV infection. AIDS, 3: 45-7, January 1989.
[32] Wolfheim JH. Primates of the World: Distribution, Abundance, and Conservation. Seattle: University of Washington Press, 1983. This monograph presents careful maps of the range of both rhesus and cynomolgus monkeys, and gives the latitudes and longitudes of the limits of their range. See especially pp. 490-1 and 475.
[33] Curtis T. Letter. Science, 256: 1260, 29 May 1992.
[34] Anonymous. "Origin of AIDS" update. Rolling Stone, 9 December 1993, 39.
[35] Baum R. Prominent AIDS researcher paints bleak outlook. Chemical and Engineering News, 71(9): 29-30, 1 March 1993. Most estimates of deaths from a full-scale nuclear war are well under a billion, and if the war never happens, the deaths will be zero. This tragedy has happened, yet this estimate of its toll (for the first few decades) by one of the foremost AIDS researchers was not even reported by the New York Times. The situation is far worse than you have been led to believe by the media, whether scientific or popular. The news they don't like, they simply ignore or suppress.
[36] Altman LK. Man dying from hepatitis is given a baboon's liver. New York Times, 11 January 1993, 12; also Altman LK. Terminally ill man gets baboon's liver in untried operation. New York Times, 29 June 1992, A1.
[37] Kimberlin RH. Some final comments on visna-maedi, aleutian disease and scrapie. In: RH Kimberlin, ed. Slow Virus Diseases of Animals and Man, North-Holland Publishing Co., 1976, see p. 386.
[38] Quoted in Curtis T. Officials Continue to Ignore Signs of AIDS-Vaccine Link, Houston Post, 19 August 1992, A1.
[39] Science, 262: 1369, 26 November 1993. Science had earlier printed several other put-downs of the theory, including their account of the Wistar Committee's conclusions, "Panel Nixes Congo Trials as AIDS Source" (Science, 258: 738, 30 October 1992), which begins: "The jury is in: No one yet knows the origin of AIDS. You thought it was ever thus?"
[40] See Ref. 7a, p. 678.
[41] See Ref. 7b, p. 577.
[42] See Ref. 7b, p. 577.
[43] See Ref. 7b, pp. 578-9. Gard administered the suspect batch of vaccine to somewhere between 20 and 1000 Swedes; I could not pin the number down any further, but my guess is that it is much closer to 20.
[44] Koprowski H. Live Poliomyelitis Vaccine (letter). British Medical Journal, 23 May 1959, pp. 1349-50.
[45] Ref. 7b, p. 579: Dr. Sabin: "This requires one little comment, and does not take up very much time.
"I would like to say that the virus was re-isolated a second time from the material that we had, using large numbers of control tubes at the same time; and that I still have the bottle I received, and I will be glad to give both the serum and the original bottle to him."
[46] Koprowski H. Historical aspects of the development of live virus vaccine in poliomyelitis. British Medical Journal, 2: 85-91, 9 July 1960. "More vaccination campaigns organized in several provinces of the Belgian Congo are raising the number of vaccinated individuals into millions" (p. 90).
[47] De Leys R, Vanderborght B, Vanden Haesevelde M, et al. Isolation and partial characterization of an unusual human immunodeficiency retrovirus from two persons of West-Central African origin. Journal of Virology, 64: 1207-16, March 1990.
[48] Vanden Haesevelde M, Decourt J-L, De Leys RJ, et al. Genomic cloning and complete sequence analysis of a highly divergent African human immunodeficiency virus isolate. Journal of Virology, 68: 1586-96, March 1994.
[49] GÅrtler LG, Hauser PG, Eberle J, et al. A new subtype of human immunodeficiency virus type 1 (MVP-5180) from Cameroon. Journal of Virology, 68: 1581-5, March 1994.
[50] The London newspaper, the Independent (Steve Connor, 3 April 1994, p. 1) reports 10 cases of the new Cameroonian virus have been found in France. Nine of the ten cases occurred in people who had formerly lived in Cameroon. (See also Loussert-Ajaka I, Ly TD, Chaix ML, et al. HIV-1/HIV-2 seronegativity in HIV-1 subtype O infected patients. Lancet, 343: 1393-4, 4 June 1994.) Apart from the Cameroonian couple who had moved to Belgium, these are the only reports outside of Cameroon and Gabon that I am aware of. The situation appears similar to, but about a decade or two behind, that described by Randy Shilts and the original HIV-1 (see beginning of discussion of point 4, in main body of this text).
If nothing else, surely this discovery of a new type of HIV-1 that exists essentially only in one small part of Africa should be enough to finally end all the talk that maybe Africa was not the origin point for AIDS. The African origin point has been evident almost from the start, but because Africans and others disliked these conclusions, they were contested. How the viruses first got into Africans has also been evident almost from the start, but because those conclusions were disliked by those who had put them there, and by their fellow scientists, they were ignored. Africans and scientists have had a common interest in obscuring the facts of AIDS' origin; thus does AIDS make strange bedfellows: Africans and their destroyers teaming up to hide the transfer, thereby assisting the transfer of other viruses, and in less direct but quite important ways assisting AIDS itself in its destruction both of Africa and of science. In many ways gays have also teamed up with their destroyers to assist in their own destruction (protests and legal action against closure of bathhouses, against testing, against contact tracing, etc.) while ignoring or ridiculing the one clear voice of sanity coming from their ranks, Randy Shilts, dead this year of AIDS. (Personify AIDS and ask: is it happy to have the bathhouses kept open or would it rather they be closed? It wants them open. It wants testing discouraged. It wants contacts unaware they are spreading the disease. Who do gays think dies when AIDS spreads? They are the victims. Victims of AIDS. And victims of themselves. Victims of a political agenda that puts gay rights ahead of gay lives. And AIDS is just so very happy to have all these extra bodies to devour. And all this extra help in getting them.) There are many other examples of victims assisting in their own destruction. Scientists are doing it in several ways and on several levels. AIDS is strong enough. It does not need any further help from us. There are enough of us who are going to die even if we start doing everything right, instead of everything wrong.
[51] There are several important reasons a new introduction is so serious, all but one of which are too complex to go into here. The one obvious reason is that one of these two viruses will be worse than the other. The difference is likely to be significant. If the first virus alone would kill a billion over the next 50 years while the second alone would kill 1.1 billion, then avoiding this second virus is worth 100,000,000 lives over just the next 50 years. (There is a time lag which I am ignoring, since the first virus at the present time has got a significant head start over the second.) There is roughly a 50 percent chance the second virus will prove to be the worse. A 50 percent chance of costing 100,000,000 lives is, to a first approximation, equal in value to a 100 percent chance of costing 50,000,000 lives. That is 2-1/2 times the 20 million currently infected, and we are only talking about the next 50 years. (And I also suspect the differences between the viruses will exceed 10 percent, perhaps very greatly.) This ignores the question of non-overlap of deaths, or rather makes the false and optimistic assumption that all of the 1 billion deaths of the milder virus are contained within the 1.1 billion deaths of the harsher. When the non-overlap portion is considered, the cost over just the next 50 years may be multiplied several or many times. (If there were no overlap at all, 2.1 billion would die from the two together, and avoiding the second would be worth 1.1 billion lives over the next 50 years.) This is only one aspect of the seriousness of a new introduction, and it is not necessarily the most important. When the increasing transmissibility of each strain, and its individual potential for evolutionary breakthroughs, and potential for interactions with other strains, are all taken into account, it is seen that each new introduction is an extraordinarily serious affair. It very strongly appears there have been at least two separate introductions of HIV-1, at least three of HIV-2 (and probably more; see Gao F, Yue L, White AT, et al. Human infection by genetically diverse SIVsm-related HIV-2 in West Africa. Nature, 358: 495-9, 6 August 1992: three have been found with only a little bit of looking), plus a separate very recent introduction of yet another variety of HIV-2, which science will have a hard time avoiding responsibility for since it has already been admitted by scientists, inasmuch as it is into members of their own profession who have been studying the monkey virus in the course of their AIDS research that it was accidentally introduced. (See Khabbaz RF, Heneine W, George JR, et al. Brief report: Infection of a laboratory worker with simian immunodeficiency virus. New England Journal of Medicine, 330: 172-7, 20 January 1994.) It will be a trivial occurrence if it is kept confined within the handful of bodies it now infects. If it escapes, it will be a new human disease and will likely claim its own megadeaths. And how will science deny its responsibility this time? Yet another new disease begun by science in its efforts to combat an older one (in turn begun by science in its efforts to combat an older one). One could have some sympathy for the plight of the scientists, now forced by the seriousness of their first mistake to risk making more, if there were any indication they appreciated the awesome seriousness of these mistakes and were making due efforts to avoid them. It is not a difficult thing to keep perhaps half a dozen or so infected scientists from spreading their new virus into others, when the probable alternative of millions of deaths is understood. There is no indication scientists have such an understanding or are making any particular efforts to keep this latest child of science from growing to its full potential. Because of confidentiality considerations, the scientists studying the case reported above don't even know the identities of the several other possible cases that have turned up, nor even precisely how many have been found (see last paragraph of above citation). There is no indication scientists consider these cases to be any more serious than another half dozen of the hundreds of needlestick cases acquired by doctors and nurses in the course of their work. The latter are new cases. The former is a new disease. There is a vast difference. Each new disease will take a different set of victims. Some of these sets will be far larger than others. Sometimes the non-overlap among sets will be far larger than others. We had better stop trying to find the worst set. It is extremely likely that at least a few of the possible immunodeficiency viruses we could transfer would, like the closely-related virus of sheep, be airborne, or otherwise casually transmissible. Some populations of African green monkeys and sooty mangabeys are infected with their own SIVs in proportions approaching 50 percent. Monkeys are short-lived species compared to human beings. We may present a significantly more inviting target for slow-virus infections, which have some difficulty with short-lived species. We are one of the two or three longest-lived species on the planet.
[52] Kreutz R, Dietrich U, Kåhnel H, Nieselt-Struwe K, Eigen M, Råbsamen-Waigmann H. Analysis of the envelope region of the highly divergent HIV-2ALT isolate extends the known range of variability within the primate immunodeficiency viruses. AIDS Research and Human Retroviruses, 8: 1619-29, 1992, see p. 1627. Though I had not seen this particular paper, I pointed out both the necessity of the reverse transfers, if the ancestor had been in human beings for 600-1200 years, as some were claiming, and their preposterousness, in a 3 May 1992 submission letter to Lancet (which submission was never even answered; nor were inquiry letters dated 31 July and 25 September 1992 ever answered): "The method used [phylogenetic tree diagrams] offers no evidence whatever that the viruses of 600-1200... years ago existed in humans rather than in simians. But if in fact, as [Robert M.] May claims, the ancestors of the HIVs were already in humans 600 years ago, then figure 4 of the Eigen paper [cited in note 11, above] clearly requires two separate implausible reverse transfers from humans into simians (from humans into chimpanzees probably some several hundred years ago and from humans into sooty mangabeys probably within the last 150 years). These reverse transfers are implausible for at least three different reasons: because you are explaining what you can already explain (the existence of lentiviruses in non-human primates) by saying they came from something you cannot explain (HIV in humans), while if you would do it in the sensible way you could explain HIV by the related SIVs of non-human primates; because the rapid growth of the epidemic and the rapid diversification of the strains both indicate that this is a new virus; and because the innocuousness of the virus in both sooty mangabeys and chimpanzees indicates their lentiviruses have been there a long time, while the fatal nature of both HIV-1 and HIV-2 indicate they are new to humanity. Indeed, HIV-1 is the most frequently fatal virus able to spread from one human being to another ever discovered (a distinction formerly held by Ebola virus, which is deadly for exactly the same reason, because it is an animal virus which the human immune system has never adapted to), and HIV-2 may well turn out to be the second most frequently fatal. A single highly implausible event can sometimes occur, but two of them are sufficient to rule his scenario out. This is particularly so when there is nothing whatever implausible about my own scenario (or if there is, no one has yet stated it, certainly not May)."
If even a few more independent virus isolates from wild-caught chimpanzees and sooty mangabeys are sequenced and added to the tree, it will emerge that still more of these implausible human-to-simian transfers are required in order to hold on to the comforting position that humans have been infected with AIDS' ancestors for hundreds of years.
[53] See the "family tree" diagram on p. 1407 of Nkengasong JN, Janssens W, Heyndrickx L, et al. Genotypic subtypes of HIV-1 in Cameroon. AIDS, 8: 1405-12, October 1994. The degree of divergence of two strains is calculated by adding up the horizontal distance of each virus back to their earliest common ancestor. When this addition is done, it is seen that the two pictured examples of this new HIV-1 type diverge to almost exactly the same degree as the maximally divergent examples of the original HIV-1 type. The conclusion that because they diverge to the same degree they were transferred at about the same time is only roughly warranted, because of their failure to correct for two large errors that occur when a change of species is encountered (see notes 11 and 54). We also need at least a few more examples to make sure none diverge still more.
[54] Perhaps Cameroon is further off the highways of world intercourse; perhaps only 1/10 or 1/100 as many were infected by the (presumed) Cameroonian vaccine; perhaps there are relevant differences in the old vs the new virus (length of incubation period, preferred cell-type in humans vs monkeys, inherent differences in rate of variation, acquired differences in rate of variation owing to the topography of the evolutionary landscape and the relative proximity of each to differently-powerful evolutionary attractors); or perhaps inaccuracies caused by the failure of the authors of the phylogenetic tree to restrict their analysis to nucleotide changes that do not cause any amino acid change, and that therefore are nearly neutral with respect to evolution, have distorted the diagram (see notes 11 and 53). One expects a sudden burst of evolution upon transfer into a new environment, so that the new virus may have been transferred more recently than first appears from looking at their diagram. There is also the possibility two closely-related varieties could have existed in even a single batch of vaccine. Since kidneys from 2 to 4 animals were used for most vaccine batches, if two infected simians (siblings perhaps) whose viruses had a common ancestor in 1958 (in their mother, perhaps) had been used for vaccine given in 1994, we would get the 1958 date when we compared human viruses arising from the one animal with viruses arising from the other. Indeed, it might even happen that a single animal had two such viruses simultaneously.
[55] Johnson PR, Fomsgaard A, Allan J, et al. Simian immunodeficiency viruses from African green monkeys display unusual genetic diversity. Journal of Virology, 64: 1086-92, March 1990.
[56] To be precise, there will certainly be some chimpanzee viruses that are more recent, but whether there are any more remote depends on whether the two human viruses have an earliest common ancestor that extends all the way back. If so, then there will be (probably very many) chimpanzee viruses equally remote, but none can be more remote. If you consider the diagram I asked you to draw, you will see that there are very many viruses that trace their ancestry back the greatest possible distance, while relatively few that trace their ancestry back only one or two steps. This is one reason the family tree diagrams are such powerful evidence: it should be easy to find viruses that trace their ancestry back the maximum distance. Thus the fact that the ancestors of the original HIV-1 are very common for recent years but abruptly stop about 1958 is very powerful evidence for a transfer at or about the point of this date. The diagram in the Nkengasong paper cited in note 53 shows quite clearly two separate recent transfers in the middle of this century, and this can be easily and unambiguously distinguished from one transfer hundreds of years ago that has just now evolved into the two separate forms. This can be done just from studying the diagrams, without even introducing the further powerful argument that a long-ago transfer implies the silly conclusion that humans infected chimpanzees and sooty mangabeys. The picture will become still clearer once a few more chimpanzee sequences are added and a few more Cameroonian sequences.
[57] And several vaccines other than oral polio vaccine are also definite possibilities. Herbert Ratner, an important early polio pioneer, has revealed extraordinary irresponsibilities and coverups in connection with Salk vaccine, many early batches of which contained, in addition to live SV-40 virus, live polio virus as well. Who knows what other viruses might have survived the inadequate killing treatment that was given to many batches or might have survived treatment that was adequate to kill polio but not some other viruses? Salk vaccine was little used in Africa because it was much more expensive than oral vaccine. But while the Western world which developed the various vaccines may not value Africans very