VIRUSMYTH HOMEPAGE


MONKEY BUSINESS OVER AIDS

By Baffour Ankomah

New African April 1998


Just as we thought the African green monkey theory about the origin of AIDS was dead and buried, American researchers have resurrected it by publishing "new evidence" in February which sought to pin the origins of AIDS on the African monkey via a "1959 blood sample" taken from "a man in Central Africa". But is this any more reliable than previous evidence? Baffour Ankomah has put it under the miscroscope and found it wanting.

The world media had a field day when the story broke on Wednesday 4 February. When AIDS made the fatal leap from ape to man, said the headline in The Times [of London].

Written by the paper's science editor Nigel Hawkes, the story said in part: "The point at which AIDS made its fatal leap from ape to man can now be more accurately fixed after the discovery of the virus in a blood sample taken from a man in Central Africa in 1959.

"The original source of the HIV-1 virus, responsible for the bulk of the epidemic, was almost certainly a chimpanzee, from which closely related viruses have been isolated.

"How HIV-1 got from chimpanzees to man is not known. Close contact with blood - perhaps while butchering a chimpanzee to eat - could have been the cause. It would have to happen only once, since the evidence is that the AIDS epidemic started with a single human case."

It was Professor Max Essex of the Harvard University who first declared in the mid-1980s that the AIDS virus had jumped over to man from the "African green monkey". Yet years later, it was proved that "the first AIDS-like viruses in monkeys had been found by Max Essex in macaques, a monkey species primarily from Southeast Asia, not Africa", New African reported in 1990.

Max Essex himself, shamed by his false theory, recanted years later and admitted that the HIV virus and the monkey virus were so different from each other that none of them "could have been the ancestor of the other in a historical past".

Now the debate has moved on. If the African green monkey is not the culprit, it must "certainly" be the African chimpanzee which, when being butchered for food, gave the virus to the man butchering it.

"It would have had to happen only once, since the evidence is that the AIDS epidemic started with a single human case", The Times science editor Nigel Hawkes wrote on 5 February 1998.

But neither Nigel Hawkes nor the American researchers could tell who this "single human case" actually was. "A man from Central Africa" was all they could conjure, leaving people to assume that "this man" coming from Central Africa could only be African. Thus "proving" that AIDS did indeed originate from Africa.

But this assumption glosses over the fact that Africa has never been an island where no foreigners had travelled or lived before. Thus, the "man from Central Africa" (said to be dead) could have been anybody - African, foreigner etc - unless the Americans are saying the blood sample has been proven to be specifically African.

Even then, how could one vouch that "this African man" did not contract the virus from one of the millions of foreigners who visited or lived in Central Africa before 1959.

As Dr Rosalind J. Harrison, the Australian-born consultant ophthalmic surgeon working in Britain wrote in New African in June 1997 (p36-39): "It is the historical inaccuracies [about the African origin of AIDS] that are more spectacular. For many centuries before the Portuguese sailed around the Cape [of Good Hope], powerful West African kingdoms conducted trade across the Sahara to the Mediterranean, and every year many thousands of West Africans made the pilgrimage to Mecca.

"On the East African seaboard, there were city states that flourished on trade between the Central and Southern African kingdoms such as Monamatapa in Zimbabwe, and Asia as far as Ming dynasty China.

"With the advent of the Portuguese began 400 years of the African slave trade, during which many millions of Africans were transported to the New World and Europe, and when African women were regularly raped from the time of capture.

"Following the demise of the slave trade came the scramble for Africa, when almost the entire continent was colonised by the European powers.

"If AIDS was the cause of a tumour as common as Kaposi's sarcoma in equatorial Africa, the disease would have spread to the rest of the world hundreds, if not thousands, of years earlier.

"Tourists from the US in the mid-1970s as the means by which AIDS reached America [is] breathtakingly naive... The Simian Immunodeficiency Virus (SIV) that have been isolated from monkeys are, like all other retroviruses, species specific - ie, in nature no monkey retrovirus normally infects a human or indeed a different species of monkeys, and there is no monkey reservoir for the HIV...

"[Yet] undeterred, scientists have estimated that SIV mutated into HIV in the last few decades. Even if such an improbable event did occur, given the colonial ties and trading links between Africa and Europe, the virus would have caused an epidemic in Europe at the same time as, or before, the epidemic in the US. Yet all the documented evidence points to an epidemic beginning in America and from there spreading to Europe."

Such common sense apparently cuts no ice with American establishment researchers and the gullible journalists who feed on their every word.

Believing absolutely in their evidence that AIDS did start with "the 1959 man" after eating an African monkey, the American researchers who made the February announcement went further to suggest in the medical journal Nature "that mass immunisation campaigns in Africa by the WHO helped to spread the disease".

This forced Jose Esparza, the vaccine development adviser for UNAIDS (the UN body that took over the WHO's AIDS programme) to defend the WHO: "There has been no new evidence," he said, "to suggest that HIV was significantly spread by the smallpox vaccination campaign. I still believe that the big social changes of the 1950s brought the virus out of the [African] jungle and into the cities. People moved more, tribal customs changed and there was more sexual contact."

So Africans began to have more sex in the 1950s?

Nigel Hawkes, The Times' science editor, suggests the virus may have infected human beings for the first time "probably in the late 1940s or early 1950s". And to great effect, he adds:

"The disease was established for decades in Africa before it was recognised as a worldwide threat."

And yet, the many Europeans and Americans who flocked to Africa for all these "decades" and had sexual contact with African women (and sometimes men), did not contract the virus until AIDS started killing Americans in the 1980s.

Back to this famous sample, there is incontrovertible evidence showing that samples frozen for too long have a high tendency of giving false positive results.

As Dr Rosalind Harrison wrote in New African in June 1997: "Evidence that false positivity was a major problem in both stored serum samples and samples taken for population studies for HIV in Africa was available from the mid-1980s, but has been largely ignored.

"Claims that early tests were unreliable but those used now can be trusted are also untenable."

Writing about the same "1959 sample" in the medical journal The Lancet in May 1986, 12 American doctors and scientists led by Dr A. J. Nahmias of the Department of Pediatrics, Emory University School of Medicine (Atlanta) admitted the following:

"The place of origin of [HIV] is controversial but most workers have suggested Africa. Most cogent to the issue has been the isolation of a related virus from the African green monkey... Because of the importance of this issue, we decided to test 1,213 plasmas obtained originally for immunogenetic studies from various parts of Africa, of which 818 had been obtained as far back as 1959.

"We appreciate that enzyme immunoessay (EIA) antibody tests on sera or plasma frozen for many years can lead to false positive results. We report here our approach to this problem and evidence for antibodies to HTLV-III [later renamed HIV-1] or a closely related virus in one plasma from Leopoldville (now Kinshasa, Zaire) in 1959."

Dr Nahmias' group said they used every sophisticated testing device available at the time - including Abbott EIA kits, direct immunofluorescence assay, Western blotting with peroxidase-labelled reagent, and Western blot with radiolabelled protein. They reported:

"According to the manufacturers, any specimen that yields an optical density (OD) on the Abbott EIA that is equal to or above the cut-off value is positive. Of the 818 plasma obtained in 1959, 752 (ie 92%) were positive using this definition while only 10% of the 277 plasmas collected in the Congo in 1982 were positive.

"While this work was in progress, we learned from Dr Schable that sera obtained by the American Red Cross which have an OD below 7x cut-off value with the Abbott kit are rarely confirmed as positive.

"So we concentrated on trying to confirm tests on plasma with an OD above 3x cut-off. None of the 1967 (Mozambique) or 1982 plasma, but 21 of the 1959 (Central Africa) plasmas fitted this category. A 10% sample of plasmas with ODs in the range 1x to 3x were tested by immunofluorescence, and all were negative.

"The 21 specimens were submitted to immunofluorescent microscopy and Western blot ensymatic immunoassay. Only one was positive by both tests. This plasma had an OD more than 7x cut-off value...

"We appreciate that when testing plasmas that were more than 25 years old, we would need to confirm any ELISA positive specimen by as many means as possible because of the risk of false positive reactions. Confirmatory tests were performed on all ratios above 3...

"We have demonstrated that at least one individual from Central Africa had been exposed to a virus similar to [HIV] more than a quarter of a century ago. THE IDENTITY OF THE DONOR IS NO LONGER KNOWN [emphasis New African's].

"Our results also suggest that the prevalence of [HIV] was very low in Central Africa in 1959. No evidence of the infection was found in sera taken in rural areas of the Belgian Congo or South Africa (1959), Mozambique (1969), the Congo (1982)."

So what evidence did Nigel Hawkes, The Times' science editor, base his assertion that "the disease was established for decades in Africa before it was recognised as a worldwide threat".

One could also ask why Dr Nahmias group stopped short of a definitive identification of the donor of the "1959 sample". By saying "the identity of the donor is no longer known", means that at some point in time his identity was known. What happened to his records? Were they wiped out? By whom? And for what purpose?

Even if the physical records no longer exist, surely somebody must have read them and known who the donor was. Was he black-African, Arab-African, white-African or Asian-African? Or was he an expatriate? Did anybody know him? Where are these people now? Can they be reached?

If the donor can be identified and his lifestyle examined, it will help greatly in tracing the origins of AIDS. In the absence of this "credible trace", any evidence pinning the origins of AIDS on Africa will remain mere speculation.

As far back as 1991, there was evidence, again published in America, showing that frozen samples were as reliable as the performances of the English Cricket team.

In the July-August 1991 issue of the US Public Health Reports, seven American doctors and researchers from the Public Health Service and the National Institute on Aging's Gerontology Research Centre, led by Dr W. Robert Lange of Baltimore, concluded definitively that frozen samples were hugely unreliable.

Their findings came at the end of a study tracing some American drug addicts whose blood samples, frozen since 1971-72, had tested positive for HIV in 1985. Dr Lange's group reported:

"Serum specimens donated from a nationwide sample of parenteral drug abusers during the period 1971-72 had previously been screened [in 1985] for HIV antibodies. Some specimens were considered to be positive to both ELISA and Western blot analysis.

"These findings have been a topic of controversy, since HIV was not thought to have penetrated at-risk populations at such an early date. This study was a follow-up of those [drug addicts] with apparent seropositivity to Western blot analysis.

"Of 10 persons followed, only one death (in 1985) was documented, and postmortem findings were inconsistent with HIV infection... The death occurred in a motor vehicle accident in June 1985, 13 years and 10 months following the [donation of the sample in Lexington in 1972]. The investigation carried out by the local medical examiner's office included a complete postmortem examination.

"The weight of the patient at the time of death (87.7 kilos) was more than 30% higher than his weight at Lexington (67.3 kilos). There was no lymphoreticular changes at autopsy, and a thorough retrospective analysis provided no evidence of either current substance abuse or HIV infection.

"Eight of the remaining [drug addicts] were traced and found to be alive and well in 1989 [some 17 years later]... The 1971-72 serum specimens were not available for retesting.

"[But] the two patients with the strongest 1985 Western blot staining patterns consented to retesting. Fresh specimens were obtained from [them], and were found to be both ELISA and Western blot negative on retesting. Their T-cell parameters were within normal limits...

"Of the seven addicts confirmed as living in 1989, none was reported to be chronically ill. One subject was incarcerated, and his family reported his health to be good."

This "miracle" (since AIDS is said to kill between 0-10 years after infection), led Dr Lange's group to conclude that:

"The earlier Western blot results [in 1985] were most likely false positives and that definitive evidence of HIV infection in the US addict population as early as 1971-72 is still lacking."

They added: "The reasons for false positivity are unclear but cross reactivity with related retroviruses may be one possibility...

"The earlier false positivity could be the consequence of either the state of the serum specimens or the test kit or assay employed. It has been suggested that artifactual findings may occur as a consequence of frequent thawing and refreezing of serum aliquots, and that frequent refreezing might affect the physical properties and serologic characteristics of the serum protein moieties."

So, now, can we take this as proof that freezing samples for a long time renders them unreliable for accurate HIV readings?

The "1959 sample" from Central Africa had been lying in the fridge for 39 long years before the recent declaration that it was the mother of all AIDS. And don't forget that the Lexington samples that fooled the American researchers in 1985 had been frozen for only 13 years (from 1972 to 1985).

Therefore, how reliable is the recent "evidence" blaming the "1959 sample" for starting the AIDS epidemic? If samples frozen for only 13 years give unreliable results, isn't it puzzling that a sample frozen for 39 long years can give accurate readings?

For an informed answer, we must go back to Dr Rosalind Harrison's June 1997 article in New African. These days, she wrote, "even 'normal' science does not function independently of its social, economic and political context.

"The days of the independent scientist conducting experiments in the study at home are long gone, and the political and economic priorities of government and industry now largely determine the allocation of funds.

"And, as scientists bring into their work their own particular cultural baggage, so too the results of their work are expected to conform with the prevailing cultural norms or vested interests.

"From the beginning of the epidemic, the political aspects of AIDS have been exceptionally prominent... Such is the murkiness of AIDS science..."

In short, we can all go to sleep safely in our beds with the knowledge that the February announcement is another "political" evidence being used to blame Africa for the origins of AIDS.


VIRUSMYTH HOMEPAGE