Excerpt from book AIDS – Origin, Spread and Healing
In the case of a female rhesus monkey, which was kept in Southborough since she was captured as a young animal in 1972, and whose cage was located next to the infected ones, a tumour developed behind one eye, in 1980. A mashed mass comprising this tumour was injected into two rhesus monkeys – MM 434-79 and MM 251-79 – in 1980. These recipients were not immunologically tested prior to the injection[1]. They therefore already could have been infected with immunodeficiency agents. The male monkey MM 251-79 became the culture medium for viruses (SIVmac-251) by which persons in Senegal (among others) were intentionally infected. This conclusion can be drawn from literature which is publicly available. The timing of the issue of publications points to an intentional misrepresentation of the spread:
August 1983: surgical transplantation of “naturally occurring” lymphoma to rhesus monkeys, including MM 251-79 in the NEPRC. MM 251-79 was slaughtered in 1982[2]. (Lymphoma did not affect one single rhesus monkey in the wild; a.).
September 1983: MM 251-79 has AIDS. Other rhesus monkeys like MM 251-79 treated with lymphoma-tissue from MM 251-79 and a further monkey – a total of 4 – catch AIDS-characteristic diseases like cryptosporidiosis, Pneumocystis carinii-pneumonia, M.a.c., TB and generalised tuberculosis[3].
June 1985: Evidence of a retrovirus in tissue of the rhesus monkey MM 251-79, which resembles the human immunodeficiency virus HTLV-III[4].
To date, this virus has been found only among a few of the thousands of rhesus monkeys in research centres, and never in a natural habitat[5].
Yet another exotic agent: the human retrovirus HTLV-I emerged in research monkeys
June 1985: serological identification and characterisation of this “new” virus in MM 251-79. Of the four rhesus monkeys with the immunodeficiency virus in Southborough, three have antibodies indicating an additional infection by a further human retrovirus – HTLV-I[6].
Preinformed researchers
June 1985: description that also in 28 out of 67 “African green healthy long-tailed monkeys caught in the wild” in research centres in Boston (USA), Cape Town (South Africa) and Frankfurt (Germany), there were antibodies against a retrovirus that was related to the human HTLV-III.
The animals were completely healthy and there was nothing to justify any investigation into AIDS agents. The reason for an examination according to the scientists: “We sought evidence for an HTLV-III-related virus in Old World primates from Africa associated with human AIDS“. HTLV-III was said to have already been present in Uganda as early as 1972[7].
The monkeys “caught in the wild” were long-tailed monkeys from Kenya and Ethiopia which had been kept for years (for example, since 1968) and to a certain extent were already the second generation in captivity in the research centers[8].
Antibodies specifically against those viruses, which originate from the Boston monkey MM 251-79
November 1985: HTLV-III related retroviruses (STLV-IIIagm) were indicated in seven out of the 27 African green long-tailed monkeys in the USA, South Africa and Germany having antibodies. They are allegedly distinguishable from the viruses in the rhesus monkeys[9].
Using the new PCR method[10] for evidence, it was possible in 1988, to determine the origin of these viruses in Boston, Cape Town and Frankfurt. The isolated viruses were exclusively SIVmac-251, the specific virus of the monkey MM 251-79 in Boston[11]. The antibodies prove that the blood samples were not contaminated by exceedingly rare viruses in each case, but that viruses were actually in the animals themselves.
A monkey from Boston, USA as sex tourist among 20 prostitutes in Dakar, Senegal?
December 1985: Antibodies were found in the blood of 20 (out of 289 = 7%) healthy prostitutes in Dakar and five healthy patients (out of 122) from a surgical hospital ward there, and when these were examined in the test tube, they reacted to the viruses which were found to be in the African green long-tailed monkeys[12].
Here again we must ask for the reason for carrying out this research: Why weren’t sick dogs and cats examined in New York and San Francisco – why healthy people in Senegal? There was not one single case of AIDS over there.
April 1986: A virus was cultivated from the blood of the infected healthy prostitutes. This could not be distinguished from the virus which the USA scientists had cultivated in the blood samples of the seven African green long-tailed monkeys[13]. This information gave rise to the impression that HIV originated from monkeys in Africa and was acquired by human beings in Africa, before spreading to NATO-states.
The new PCR evidence method also revealed the culprits in this case. Here too, Kanki, Essex and colleagues had cultivated in the blood samples from Senegal[14] precisely the specific virus from the one rhesus monkey MM 251-79 in Boston. The antibodies prove that it was not the blood samples that were contaminated by the exceptional rare viruses, but that viruses originating from Boston had actually been present in the persons in Dakar. The prostitutes had undergone previous regular treatment for sexually transmitted diseases.
This retrovirus STLV-III (= SIVmac-251) strikes and replicates itself in cultures of human lymphocytes[15] – it is, therefore, a human (“H”) Immunodeficiency Virus. The prostitutes were still healthy four years later. The proportion of HIV-2 (= HTLV-IV)-infected prostitutes increased annually by 0.5%- to a bare 10% respectively remained unchanged in eight years.[16] Infection with the virus occurred irrespective of the time these women worked as prostitutes[17].
Kanki and colleagues maintain that antibodies against the immunodeficiency virus of the African green long-tailed monkeys were found in one human blood sample from Dakar, which had been taken already between 1975 and 1976[18]. But the source quoted, which should have described the origin of the sample, did not indicate the domicile of the donor[19].
It is most unusual to omit this very important information in an epidemiological study.
February 1987: From among roughly 30 prostitutes and 36 prisoners in three towns in the Ivory Coast, antibodies were discovered in 1986 against those retroviruses found in the Senegalese prostitutes[20](= SIVmac-251; a.).
A third human retrovirus
July 1986: Report that a new human retrovirus was found from two AIDS patients from West Africa, which was recognised by antibodies, fighting against the immunodeficiency virus in rhesus monkeys from the NERPRC. In other words, the two viruses were very closely related[21].
However, only one of the two showed the symptoms corresponding to the actual AIDS-definition. In 1983, the patient had begun to suffer from the onset of diarrhoea, weight loss and enlarged lymph nodules. Because of this, he had come from his home country Guinea-Bissau to a hospital in Lisbon for treatment. The second patient (“ROD”) was suffering from fever and diarrhoea accompanied by weight loss in January 1982. He therefore was sent from his homeland – the Cape Verde Islands – in June 1983 to the Claude Bernard AIDS-specific hospital in Paris. At that time, he had no more clinical symptoms and had almost regained his original weight. The infection of the brain with toxoplasmosis, as claimed by the author Clavel, can only be supposed. Such could only have been diagnosed after death. The recovery of the person who returned to the Cape Verde Islands, contradicts this diagnosis. The virus from “ROD” resembles closely the SIVmac-251 virus, but was actually different.
The virus-envelopes but not the cores, had identical antigen properties[22]. This HIV-2 virus was most frequently spread in parts of the population of the Federal Republic of Germany. It was found in 4% of “Africans” living there. In “Africans” in West Africa it was found in 0.6%, and in Central Africa in 0.1%[23]. In Germany it was found in blood samples of the year 1984[24]. Necessary cofactors leading to the efficacy of the virus, seem to be missing there. The infected persons were healthy and had no immunodeficiency.
HIV-2 ROD which was obtained from the blood of the healthy patient “ROD” became prototype of the HIV-2 viruses.
Theory of sexual intercourse between human beings and monkeys in West Africa
May 1986: Retroviruses which were identical with the STLV-IIImac (= SIVmac) of the captured rhesus monkeys, were indicated in leprous, but otherwise healthy, cebus monkeys in the Primate Research Center New Orleans, USA and also in those rhesus monkeys which had been transplanted with the lepra-tissue from these cebus monkeys and which subsequently suffered from AIDS[25].
July 1986: 14 of the 15 cebus monkeys captured and examined carry this SIVsmm-virus without showing any clinical symptoms. It is unknown, whether it is the same as SIVmac-251[26].
June 1989: three years after the description of the retroviruses (SIVsmm) in captured, healthy cebus monkeys in USA research centres, the head of research, PN Fultz, maintained that these viruses had also been isolated in cebus monkeys living wild in “West Africa”.
Silence about the numbers, place and time of this evidence. But:
this (alleged) occurrence outside research centres together with an (alleged) extensive spread of HIV-2 ROD (= Cabo Verde occurrence) amongst people in West Africa was said to be an indication that 30 to 40 years ago, retroviruses from a cebus monkey must have penetrated a human organism and then had transformed itself into the HIV-2 retrovirus. As an alternative, the USA scientists state, that HIV-2 ROD had passed from human beings to monkeys and had changed in the latter[27]. They don’t even discuss the possibility that HIV could have been transmitted by insects, parasites, birds, fishes, by sea-men and tourists to people and animals in “West Africa”.
How could human beings have infected monkeys with HIV? To date, there is no indication whatsoever that West African cebus monkeys living in the wild, consume intravenous drugs, transfuse untested blood pints, use contaminated blood products, or frequently use unsterilized injection syringes. These possibilities explaining infection with the human virus, obviously do not apply to animals. Since human beings do not bite monkeys, the research authors impertinently expect us to believe transmission from a human being to an animal by way of sexual intercourse between a West African person and a wild 24 inch tall monkey.
How could human beings have acquired SIV from monkeys? Since, of the 15 million or so HIV-infected persons, there is not a single case of transmission via saliva (the exception was supposed to be a dentist from the USA – see chapter 3.3.8) or through biting[28], this possibility must also be rejected for West Africa with regard to transmission from animal to human. Here too, we will have to imagine the transmission of the SIVsmm from a little monkey to a West African person as an hurly-burly circus stunt in a tree-top.
A fourth human retrovirus
The alleged precursor virus of HIV-2, HIV-2-D205 was also found in Germany in a healthy woman from Ghana[29]. This virus is a further human retrovirus.
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