Edward Hooper’s unpublished letter to the editor of Nature in response to John Moore’s review (Nature, 23 September 1999)
September 27, 1999.
Dear Mr Campbell,
I read with great interest John Moore’s review of my book, The River. Might I point out that it contained a number of errors? I would appreciate the opportunity to correct these in your pages.
Given the significance that the hypothesis that the world’s largest pandemic has an iatrogenic origin bears for the scientific community, and the importance that the issue be not only dealt with fairly, but seen to be dealt with fairly, I hope that you will consider providing me with sufficient space (which, in this instance, turns out to be an equal amount to that occupied by Dr Moore!) to respond to his arguments, and (where necessary) to set matters straight.
If you wish to trim the letter, and would like to do this with my cooperation, I would be very glad to help if I can.
With best wishes,
Edward Hooper.
Damning The River.
Dear Sir,
Dr John P. Moore’s review of my book, The River [Nature 401, 325-326, 1999] gives a good indication of just how threatened some scientists are now feeling by the so-called polio vaccine theory of origin of AIDS.
A little context is needed. One month ago John Moore, who is a vocal opponent of the hypothesis, wrote the following: “The polio vaccine theory of the origin of AIDS is something that is only believed in by the lunatic fringe – It is sheer unadulterated nonsense, and not worth a moment of a serious scientist’s time.”
Despite being a serious scientist, Dr Moore has clearly thought more about the theory since then, for his review concedes that The River “is, in many ways, superb – scholarly, thoroughly researched – and deserves, even demands, to be taken seriously.”
However, having lavished praise on the generalities, when it comes to the specifics he (like some polio vaccines) reverts. First, he inappropriately likens the central hypothesis of the book to a well-known conspiracy theory. And then he attacks the hypothesis, but all too often by misrepresenting what it involves.
He claims that “a chain of events is outlined in which each link is weak”. The first weak link, he says, is my proposition that sick chimpanzees housed at Lindi camp in the Congo in 1957-8 might have been infected with a primate immunodeficiency virus (PIV) ˆ because, he points out, there is no evidence that PIV causes disease in chimps. This misses the point. Of the 400-odd chimps that Dr Koprowski and his Belgian colleagues used for polio research at Lindi in the twenty-one months from June 1956 to February 1958, several (eight to twelve) would likely have been infected with PIV, on the basis of our existing knowledge of seroprevalence in chimps, and further viral spread may have occurred within the camp, through animals sharing cages. My hypothesis is that the kidneys of some Lindi chimps were used for tissue culture to grow Dr Koprowski’s experimental oral polio vaccine, CHAT. In practice, overtly sick animals would clearly have been rejected, but it matters little, for any donor animal, healthy or sick, could have been PIV-infected.
Surprisingly, Moore then asserts that the chimp kidneys dispatched to Philadelphia during this period were sent not to Koprowski’s Wistar Institute, but to another institute doing hepatitis research, and adds that the surviving Philadelphia- and Congo-based scientists all deny that polio vaccines were ever made from chimp kidneys. Again, not quite correct. According to two of my cited sources, chimp kidneys were sent specifically to the Wistar, and one of the Belgian scientists of the era initially told me that chimp kidneys had been used to produce CHAT vaccine, only to retract minutes later. Furthermore, virologists from the hepatitis laboratory were collaborating with Koprowski on his polio vaccine studies at Clinton, a nearby women’s prison.
Since The River went to the printers, I have visited Kisangani (formerly Stanleyville) and interviewed a man who worked at Lindi in the fifties, who told me of watching experiments in which chimps were sacrificed in groups of five or six, and large organs removed from their bodies. According to this careful witness, this happened not just a few times (as for the hepatitis research), but “from the beginning of Lindi camp to the end” (1956 to 1959).
Dr Moore doubts that chimp kidney cultures “would produce much [PIV] and that enough of this would survive storage and shipment” and make it through to the final vaccine. In fact, there is no scientific reason why contaminant PIV would not survive at low levels, for CHAT was a live vaccine, which could not be denatured. Given that CHAT was then fed to over a million persons from the Congo, Rwanda and Burundi, there is every reason to suppose that some vaccinees (mainly infants and the already immunocompromised) would have become infected.
Although Moore concedes that the first authentic HIV-1 sequence cropped up in 1959 in Leopoldville (the Congolese capital, and the site of a large CHAT vaccination), he doubts that the transfer to humans could have occurred as late as 1957 (when the vaccination campaigns began). He thinks it more likely that the transfer occurred a few decades earlier, as a result of a local hunter getting infected when butchering a chimp. He does not seem mindful of the substantial coincidence that this would require, and ignores the fact that humans have been butchering chimps (without, it would seem, causing AIDS) since the two species diverged. By contrast, a retrovirologist who has read The River recently told me that the CHAT theory of origin of AIDS “is indeed consistent with the phylogenetic evidence”.
Dr Moore expresses doubt that the African CHAT vaccinations of 1957-60 would have taken fifteen or so years to spark the AIDS epidemic that first became visible in the seventies. In fact, this is exactly the period it would have taken for vaccinated infants and young children to reach maturity, and to spread the virus sexually. Furthermore, he fails to mention the extensive evidence provided in The River that fatal immunodeficiency diseases (related to Klebsiella pneumoniae, tuberculosis and generalised herpes) occurred, from 1958 onwards, in many of those living in vaccinated areas.
Most importantly, Moore ignores the correlations I establish between the very first instances of HIV-1 infection and AIDS in Africa, and the CHAT campaigns. Remarkably, over 64% of all clinically plausible and serologically confirmed AIDS detected in Africa, as a whole, prior to 1981 (the year when the condition was recognised in the USA) are linked to towns where CHAT was fed, as are over 87% of all confirmed pre-1981 HIV-1 infections in that continent.
Instead, he informs us: “Hooper cannot prove what he proposes and many of his arguments are highly speculative”. While I would (for now) agree with the first clause, the second seems inappropriate.
None the less, I would like to thank Dr Moore for calling for the remaining records of CHAT vaccine to be released, and the remaining vaccine stocks to be tested (though I would suggest they be tested not only for PIV, but also for the mitochondrial DNA of the host). I also welcome his support for the book’s warning about similar medical disasters which may be waiting in the wings, such as xenotransplantation. And I wholeheartedly endorse his conclusion that “even if the OPV-HIV link were correct, neither Koprowski nor anyone else would be to blame”. Nobody is trying to scapegoat Dr Koprowski or any of his American or Belgian colleagues, all of whom were clearly trying to save lives. Indeed, if this hypothesis does ever come to be proved, then they – as well as the millions who have gone on to become infected with HIV – will be deserving of considerable sympathy.
John Moore ends by saying that the case is “Not proven”. I would tend to agree. However, as someone with the interests of the scientific community at heart, I would like nothing better than for members of that community with the appropriate experience, equipment and knowledge to carry this investigation forwards.
Yours sincerely,
Edward Hooper.