1999.02.27 Monkey Business Again?
In view of the latest "proof" of the origin of AIDS in African chimpanzees, and the purported concomitant demise of all conspiracy theories of an artificial origin, such as that of the late Prof. Jakob Segal, it may be instructive to read what he had to say about the first monkey theory.
Fourteen years ago, it was not chimps but green monkeys.
The following is a translation of part of a chapter of Segal's last book, which, incredibly, has never been translated into English (AIDS Ist Besiegbar, 1995). Segal died in 1996. Nor has another, purely medical book, called AIDS: Zellphysiologie, Pathologie und Therapie, 1992, which suggests a cure. Both are available from Verlag Neuer Weg, Kaninenberghöhe 2, 45136 Essen, Germany.
I have slightly abridged the original. - Michael Morrissey, Feb. 27, 1999.
The Legend of the Green Monkey
1. Monkey Business
The notion that AIDS could be the result of experimental genetic engineering has been around almost from day one. It was discussed at the 1984 conference of the American Association for the Advancement of Science, and subsequently reported in the journal Science, without a word of rebuttal. Behind closed doors, most American experts were quite open to the possibility. But this dangerous speculation had to be suppressed. In order to distract attention away from this line of investigation, two theories were created: the legend of the African green monkey, and the myth of the isolated African village.
But first the propagators of these falsehoods had to be legally protected. A Supreme Court decision on April 16, 1985 established the right of the CIA to keep the names of scientists who worked for them secret. Within the same month, Max Essex published his green monkey story.
Since this was propaganda, not a real scientific theory, Essex did not publish it in any scientific journal. He mentioned it for the first time at the international AIDS conference in Atlanta in April 1985. He had been invited to give a special lecture, outside the regular program. Although all other participants had to submit an abstract of their talk, Essex didn't bother. He was just testing the waters. The real campaign started on August 12, 1985, when the story was reported on TV and in the New York Times and Der Spiegel. He didn't speak about it again until November, at the Brussels conference on "African AIDS." This time he did bring along a one-page summary, and a poster. But this is all we have, since Essex, contrary to normal practice, has never published any details in any scientific journal.
Essex and his colleague (Kanky et al.) reported on a group of 104 green monkeys (Cercopitecus aethiops) that had just been captured and were completely healthy, except that 57 of them carried an apparently non-pathological retrovirus. This virus gave a cross-reaction with [? "gab eine Kreuzreaction mit] HIV, the AIDS virus, in the 5' region of the genome. This is not surprising, since we know the gag-gene proteins, which are located in this 5' region, occur with a certain uniformity in the various groups of retroviruses. No attempt was made to compare the 3' region of the genomes, which is where the differences between HTLV-I and HIV are most apparent. On the basis of this dubious finding, the authors declared that the monkey virus contained all the important proteins of HIV, and that one could hardly tell them apart. Since Gallo had already named the AIDS virus HTLV-III, Essex baptized his new virus STLV-III (S for simian), in order to emphasize the identify he quite arbitrarily assumed existed. He concluded that the virus had been transferred to a human (hunter) through biting or scratching, and there spontaneously developed into HIV and caused the epidemic.
To strengthen their argument, the authors declared that they had found the green monkey virus (STLV-III) among many healthy Africans, in fact about 90% of those examined. Furthermore, to show that the monkey virus could in fact cause AIDS in man, the authors reported that they had found both HIV and the monkey virus in 17 of 32 American AIDS patients (i.e., 53%).
This is illogical. On the one hand, we are told that the monkey virus becomes the AIDS virus as soon as it is transferred to humans. At the same time, we are told that 90% of the healthy Africans examined carried the monkey virus, i.e. with no signs of AIDS, and that 53% of the American AIDS patients had both viruses.
We are supposed to conclude that 53% had AIDS because of the monkey virus. Where, then, did the other 47% get it? Were there two different sources of AIDS?
Essex contradicts himself on the supposed identity of the two viruses. He says he identified both viruses in 53 percent of the AIDS patients. That means the serological reactions of the two viruses are so different that the antibodies formed against them can be clearly differentiated, even when they are right next to each other in the blood. The similarity, then, cannot be very great.
Worst of all, Essex claims that a parasitic, non-pathogenic virus in green monkeys, that is, a virus genetically adapted to its host, "undergoes a genetically fixed heredity of acquired characteristics", which contradicts all the laws of modern genetics. [Segal is apparently quoting Essex: ..."erleide eine erblich fixierte Vererbung erworbener Eigenschaften." I do not have the original. I think Segal means that what Essex said or wrote is nonsense. --Transl.] At this point it became clear to us that this theory was nothing but a propaganda ploy.
2. Science Against Legend
Without mentioning the green monkey "theory" directly, the WHO stated officially in 1985 that some of the T-lymphotropic monkey viruses have an insignificant similarity with LAV/HTLV-III (former name for HIV). There could not have been a clearer refutation of the green monkey theory.
In the fall of 1984 and the spring of 1985, a group of Japanese researchers, among them such well-known experts as Watanabe, Komuro and Toshiki, published two important papers. The authors had isolated five virus strains from different species of monkeys, and cultivated them. Three came from the Japanese rhesus monkey, one from an African chimpanzee, and one from an African green monkey. This shows, incidentally, that Essex was not the first to isolate the green monkey virus, and had no right to give it a name.
The Japanese researchers compared the genomes of these viruses with that of HTLV-I. They used the hybridization method as well as the direct comparison of nucleotide sequences. The results of both investigations were the same.
All the HTLV-I strains that had been isolated were almost identical, varying by less than 1%. The five different monkey viruses were also very similar to each other, and also similar to HTLV-I, the difference being about 10% in the various parts of the genome. As an example, the Japanese team compared the 3' end of the HTLV-1 genome with the 3' end of the virus from the rhesus monkey. They were 90% identical.
As we have already mentioned, Alizon and Montagnier have shown that the genome of HTLV-I is quite different from that of HIV, far too different for HIV to have developed naturally from HTLV-I. And if the monkey viruses are so closely related to HTLV-I, as the Japanese research tells us, it makes no sense to assume that such a virus could be transformed into HIV simply by changing hosts.
The Japanese research shows us that the various STLV virus (simian T-cell lymphotropic viruses) are closely related to each other, and to HTLV-I. HTLV-I and BLV (bovine leukemia virus) are also related. All of them, including HIV, come from a common ancestor virus, which has probably died out. But HTLV-III/HIV constitutes a completely separate branch of the tree. It is thus impossible for an STLV virus to have been transformed into HIV by entering the human body.
The Japanese findings, and others that were published around the same time disprove conclusively the green monkey theory. This was the solid scientific basis of the WHO's statement in 1985. This so-called theory should never have seen the light of day. The Japanese work had already appeared in 1984 in the journal Virology, five months before the Atlanta conference where Essex first introduced his idea, and nine months before it hit the mass media. Essex is a virologist, so he must have been aware of the leading journal in his field. Even if he missed that issue, surely his colleagues would have informed him.
The only thing that Essex proved is that both the African green monkey as well as the North American human population very often carry a non-pathogenic virus, and that this virus may be more common among the inhabitants of central Africa. Non-pathogenic viruses are common in humans. CMV (cytome-galo virus) is found in about 40% of Europeans (according to the country). It causes illness only under certain circumstances, for example, in some cases of full-blown AIDS.
The fact that we find a virus in man as well as in animals should not surprise us. Rabies attacks people, dogs, foxes, cats, deer, and other animals. This is elementary epidemiology, and only Essex sees this fact as so terrifying.
At the second international AIDS conference, in Paris in June 1986, no less than five research groups presented their findings comparing the green monkey virus with AIDS. They investigated the structure of the viruses, their enzyme activity, the organization of the genome, and the antibodies that formed in infected organisms. They all came to the same conclusion--that the development of a virus from the HTLV group into the AIDS virus was impossible.
But not until six months later did Essex's group concede defeat. They hid this concession in a jungle of technical detail (Hirsch et al., 1986), but including the following: "The limited homology between the STLV-III AGM (African Green Monkey) and HTLV-III/LAV leads us to the conclusion that neither one could be a direct ancestor of the other in historical time." These words suffice to bury the green monkey theory once and for all.