The Durban Declaration of HIV as the Cause of AIDSgreenspun.com : LUSENET : Grassroots Information Coordination Center (GICC) : One Thread
Endorsed by a coalition of 5,000 of the world's leading scientists and doctors that incudes 11 Nobel Prize laureates
Seventeen years after the discovery of the human immunodeficiency virus (HIV), thousands of people from around the world are gathered in Durban, South Africa to attend the XIII International AIDS Conference. At the turn of the millennium, an estimated 34.3 million people worldwide are living with HIV or AIDS, 24.5 million of them in sub-Saharan Africa (1). Last year alone, 2.8 million people died of AIDS, the highest rate since the start of the epidemic. If current trends continue, Southern and Southeast Asia, South America and regions of the former Soviet Union will also bear a heavy burden in the next two decades.
AIDS spreads by infection, like many other diseases, such as tuberculosis and malaria, that cause illness and death particularly in underprivileged and impoverished communities. HIV-1, which is responsible for the AIDS pandemic, is a retrovirus closely related to a simian immunodeficiency virus (SIV) that infects chimpanzees. HIV-2, which is prevalent in West Africa and has spread to Europe and India, is almost indistinguishable from an SIV that infects sooty mangabey monkeys. Although HIV-1 and HIV-2 first arose as zoonoses (2)-infections transmitted from animals to humans-both now spread among humans through sexual contact; from mother to infant; and via contaminated blood.
An animal source for an infection is not unique to HIV. The plague came from rodents and influenza from birds. The new Nipah virus in Southeast Asia reached humans via pigs. Variant Creutzfeldt-Jakob disease in the United Kingdom is identical to 'mad cow' disease. Once HIV became established in humans, it soon followed human habits and movements. Like many other viruses, HIV recognizes no social, political or geographic boundaries.
The evidence that AIDS is caused by HIV-1 or HIV-2 is clear-cut, exhaustive and unambiguous, meeting the highest standards of science (3-7). The data fulfil exactly the same criteria as for other viral diseases, such as polio, measles and smallpox:
It is unfortunate that a few vocal people continue to deny the evidence. This position will cost countless lives.
- Patients with acquired immune deficiency syndrome, regardless of where they live, are infected with HIV (3-7);
- If not treated, most people with HIV infection show signs of AIDS within 5-10 years (6, 7). HIV infection is identified in blood by detecting antibodies, gene sequences or viral isolation. These tests are as reliable as any used for detecting other virus infections;
- People who receive HIV-contaminated blood or blood products develop AIDS, whereas those who receive untainted or screened blood do not (6);
- Most children who develop AIDS are born to HIV-infected mothers. The higher the viral load in the mother, the greater the risk of the child becoming infected (8);
- In the laboratory, HIV infects the exact type of white blood cell (CD4 lymphocytes) that becomes depleted in people with AIDS (3-5);
- Drugs that block HIV replication in the test tube also reduce viral load in people and delay progression to AIDS. Where available, treatment has reduced AIDS mortality by more than 80% (9);
- Monkeys inoculated with cloned SIV DNA become infected and develop AIDS (10);
- HIV causes AIDS (5); and
- Further compelling data are available (4).
In different regions of the world, HIV/AIDS can show altered patterns of spread and symptoms. In Africa, for example, people infected with HIV are 11 times more likely to die within 5 years (7), and more than 100 times more likely than uninfected people to develop Kaposi's sarcoma, a cancer linked to yet another virus (11).
As with any other chronic infection, various factors have a role in determining the risk of disease. People who are malnourished, who already suffer other infections or who are older, tend to be more susceptible to the rapid development of AIDS following HIV infection. However, none of these factors weakens the scientific evidence that HIV is the sole cause of the AIDS epidemic.
In this global emergency, prevention of HIV infection must be our greatest worldwide public health priority. The knowledge and tools to prevent infection are available. The sexual spread of HIV can be stopped by mutual monogamy, abstinence or by using condoms. Blood transmission can be prevented by screening blood products and by not reusing needles. Mother-to-child transmission can be reduced by half or more by short courses of antiviral drugs (12, 13).
Limited resources and the crushing burden of poverty in many parts of the world constitute formidable challenges to the control of HIV infection. People already infected can be helped by treatment with life-saving drugs, but the high cost of these drugs puts these treatments out of reach for most of the world. It is crucial to develop new antiviral drugs that are easier to take, have fewer side effects and are much less expensive, so that millions more can benefit from them.
There are many ways of communicating the vital information on HIV/AIDS, and what works best in one country may not be appropriate in another. But to tackle the disease, everyone must first understand that HIV is the enemy. Research, not myths, will lead to the development of more effective and cheaper treatments, and, it is hoped, a vaccine. But for now, emphasis must be placed on preventing sexual transmission.
There is no end in sight to the AIDS pandemic. But, by working together, we have the power to reverse its tide. Science will one day triumph over AIDS, just as it did over smallpox. Curbing the spread of HIV will be the first step. Until then, reason, solidarity, political will and courage must be our partners.
1. UNAIDS. AIDS epidemic update. December 1999. www.unaids.org/hivaidsinfo/documents.html
2. Hahn BH, Shaw G M, De Cock KM, and Sharp PM (2000). AIDS as a zoonosis: scientific and public health implications. Science 287. 607-614.
3. Weiss RA and Jaffe HW (1990). Duesberg, HIV and AIDS. Nature 345. 659-660.
4. NIAID (1996). HIV as the cause of AIDS. www.niaid.nih.gov/spotlight/hiv00/default.html
5. O'Brien SJ and Goedert JJ (1996). HIV causes AIDS: Koch's postulates fulfilled. Current Opinion in Immunology 8. 613-618.
6. Darby, SC and others, (1995). Mortality before and after HIV infection in the complete UK population of haemophiliacs. Nature 377. 79-82.
7. Nunn, AJ and others, (1997). Mortality associated with HIV-1 infection over five years in a rural Ugandan population: cohort study. British Medical Journal 315. 767-771.
8. Sperling, RS and others, (1996). Maternal viral load, zidovudine treatment, and the risk of transmission of human immunodeficiency virus type 1 from mother to infant. New England Journal of Medicine 335. 1678-80.
9. Centers for Disease Control and Prevention (CDC). HIV/AIDS Surveillance Report 1999; 11. 1-44.
10. Liska, V and others, (1999). Viremia and AIDS in rhesus macaques after intramuscular inoculation of plasmid DNA encoding full-length SIVmac239. AIDS Research & Human Retroviruses 15. 445-450.
11. Sitas, Fand and others, (1999). Antibodies against human herpesvirus 8 in black South African patients with cancer. New England Journal of Medicine 340.1863-1871.
12. Shaffer N and others, (1999). Short course zidovudine for perinatal HIV-1 transmission in Bangkok Thailand: a randomised controlled trial. Lancet 353. 773-780.
13. Guay LA and others, (1999). Intrapartum and neonatal single-dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: HIVNET 012 randomised trial. Lancet, 354. 795-802.
HIV and Hepatitas
-- spider (email@example.com), March 08, 2001
Monkey Study Shows Promise for AIDS VaccineWASHINGTON (Reuters) - Researchers reported
on Thursday that an AIDS (news - web sites)
vaccine kept monkeys healthy for months after
infection with an HIV (news - web sites)-like
virus, and scientists plan to begin testing
early next year whether the same approach
works with people.
-- spider (firstname.lastname@example.org), March 08, 2001.
08/03/2001 10:25 - (SA) Aids to reap a grim harvest
Bothaville – Aids will have a huge impact on South African commercial agriculture within the next 25 years.
Commercial farming areas are likely to depopulate. By 2010 Aids- related deaths in the farming sector are likely to increase five-fold over natural deaths and by 2025 the South African population will show static growth.
This sobering message was delivered on Wednesday to the country’s wheat farmers at the Wheat SA congress.
Speaking at the congress, Dr Jan du Plessis, a well-known political analyst, said the Aids epidemic has assumed the proportions to destroy South Africa. Current infection rate figures are even more staggering when taken in comparison to just a decade ago, when, in 1990, just 0.7 percent of the total population was infected with the virus.
"By 2025 the average life expectancy of South Africans will be slashed from 70 years to 35 years as a result of Aids.
"Do you know how many people have to die to arrive at those figures? It's horrific.
"We are viewing Aids as a disease. You, who are active in agriculture, should not regard it as a disease, but rather consider its effects. Aids changes labour and labour laws as more and more people become ill.
Du Plessis believes the effects of the Aids pandemic are likely to be similar to those of the Black Plague which ravaged Europe in the 14th Century, leaving 30 million dead.
"After the plague, labour practices changed as the labour market had shrunk. Their farming equipment was improved. Technological innovation will have to be managed in South African agriculture. It is a painful process, but necessary," Du Plessis warned.
In a comprehensive report over the sustainability of wheat production in South Africa introduced at the congress, well-known market analyst Dr Lawrence Schlemmer said the population of the Free State will plummet by 70 percent over the next 25 years as a result of Aids.
This constitutes the highest expected population reduction of all regions in the country, a full six percent higher than the Boland’s expected decline of 64 percent.
Rural populations in Gauteng, North and the Western Cape would also decline considerably, Schlemmer noted.
He added that the social, political and economic effects of the Aids pandemic on South Africa - projected as being worse than anywhere else in the world - will be no less than calamitous.
The South African population should stand at 48.3 million by 2015 and by 2025 in the region of 48.9 million.
-- Martin Thompson (email@example.com), March 08, 2001.
It's interesting that the court case in
South Africa to let Africans make their
own AIDs medicine was postponed now that
Merk and other drug companies consented
to lower the price of these drugs to poor
-- spider (firstname.lastname@example.org), March 08, 2001.
Good God, somebody has got to say something. Please read Peter Duesberg's book, Inventing the Aids Virus. He categorally crushes each one of these claims that HIV is the cause of aids. There are many doctors today who are trying desperately to get the message out about this disease, but the size of the World Health Organization and Aids International Conference have a weighted advantage which they are weilding to keep the truth about aids unknown to an unsuspecting public. Please read this book, it will grab your interest on the very first page and change your life in a most positive way.
-- Ken (N4Wind@aol.com), March 08, 2001.
Indeed. Peter Duesberg's book, Inventing the AIDS Virus is "must read" for those that want to find any truth in the AIDS debate.
Thank God that the President of South Africa has had the guts to confront the multi-billion dollar AIDS industry and seek the truth. Fortunately many people here in the U.S. have begun resisting the "HIV causes AIDS" mantra.
AIDS drugs are the often real killers of the people taking them. African nations are suffering mainly from malnutrition and the stress caused by homelessness, warfare, and rapid destruction of culture. The diseases in Africa (and the AIDS diseases) are not new. They are just called AIDS when a test-- found so often in error as to be unreliable- - identifies HIV antibodies (not HIV itself by the way). Without those antibodies, the person "just" has eg. tuberculosis.
AIDS is a definition, not a disease. Of course some of the underlying diseases are just as communicable as they were before the AIDS definition arose. But HIV has nothing to do with it.
-- Neil Ruggles (email@example.com), March 09, 2001.
I have been researching extensively -- reading scientific papers to the best of my ability, rather than just news reports and "declarations." Ask me if I would fear being "infected" with this "virus."
Ran across a quote, something to the effect of, "If you look at both sides of a story, you realize there is more to the story than both sides." With that in mind, you might want to check out what these "few vocal" people are saying. http://www.virusmyth.net is a good start. What could it hurt?
-- L. Hunter Cassells (firstname.lastname@example.org), March 09, 2001.
Thank you for publishing material relating to the so-called "dissident" view that HIV does not cause AIDS and AIDS is a long-term breakdown of the immune system rather than an infection by a single agent. The HIV/ AIDS model is irrational on its face and has been sustained as long as it has only by a corrupt scientific establishment willing to rewrite its own rules: i.e., redefining viral "isolation" so it no longer requires isolation of an intact, infectious virus; redefining Koch's Postulates, the standard test of whether a microbe causes a disease, by allowing the use of PCR tests — invented, BTW, by a scientist who rejects the HIV/AIDS model — instead of actual viral isolates; and redefining an antibody response (which is what a so-called "HIV- positive" test is), which for genuine viral diseases means IMMUNITY, to mean instead the virtual certainty that you will get the disease and die from it.
Several alternative AIDS sources have published rebuttals to the Durban Declaration. Here's the one I find most appropriate for this debate because it is comprehensive and also concise (which not all the responses have been):
PERTH GROUP COMMENTARY ON THE DURBAN DECLARATION August 11th 2000 REJECTED BY NATURE September 12th 2000
Below is the Perth group commentary on the Durban Declaration. This was sent to the editor of Nature with the following covering note:
Dear Dr. Campbell,
Please find attached comments by my group to the Durban Declaration.
The reasons prompting this submission are two-fold. Firstly, the Durban Declaration was a response to President Mbeki's decision to host a selected panel of scientists to debate the HIV theory of AIDS in South Africa in May and July this year. My group attended the second meeting and made an invited presentation on "HIV Testing and Surveillance" (www.deltav.apana.org.au/~vturner/aids).
Your correspondent in South Africa, Dr. Michael Cherry, was an observer at all proceedings over the two days of the meeting, including the subcommittee which deliberated and then resolved to perform experiments to prove or disprove the specificity of the HIV antibody tests for proving HIV infection. This outcome was agreed to by Professor William Makgoba of the Medical Research Council of South Africa, Dr. Helene Gayle of the US Centers for Disease Control, as well as Professor Barry Schoub and Dr. Caroline Williamson, both two South African experts in virology.
For some reason, news of this event was not conveyed to the readership of Nature, although Dr. Cherry was also present at the post-meeting press conference where this was made public. At the press conference Dr. Gayle repeatedly said there was a need to get "back to basics". Our attached comments document the scientific arguments we put to the meeting which assisted the Panel in reaching its decision to conduct these experiments. (Which are currently being designed in various centres).
Second, the Durban Declaration was presented by 5000-plus scientists/ physicians as their scientific rationale for upholding the HIV theory of AIDS. Using data over the same time span we argue the contrary.
As President Mbeki himself observes, there are many scientists who, from many angles, present scientific arguments questioning the HIV theory of AIDS. Everyone acknowledges the generous contribution of space Nature has provided in the past to address matters raised by Peter Duesberg. However, my group's papers, including one published in Nature Bio/Technology in 1993, raise many questions totally removed from Duesberg. These concern the basic tenets of the HIV theory: including, for example, the antibody tests and HIV isolation. Such questions have never been addressed let alone answered.
We realise that space is a constant premium but we would be most willing to shorten this contribution. Alternatively, perhaps you might consider a precis and, as with the Durban Declaration, make use of your website for the bulk of the writing.
Eleni Papadopulos-Eleopulos Fax +618 92241138 Voice + 618 92242500
On 13th of September we received the following Fax:
Nature Editorial Porters South Crinan Street London N1 9XW United Kingdom
Dr E Papadopulos-Eleopulos Tel: +44 (0)20 7833 4000 Department of Medical Physics Fax: +44 (0)20 7843 4596/7 Royal Perth Hospital Perth Western Australia
12 September 2000-09-14
Re: E Papadopulos-Eleopulos et al "Commentary-The Durban Declaration"
Thank you for submitting your manuscript, which we regret we are unable to publish.
It is Nature's policy to decline a substantial proportion of manuscripts without sending them to referees, so that they may be sent elsewhere without delay. Decisions of this kind are made by the editorial staff when it appears that papers are unlikely to succeed in the competition for limited space.
Among the considerations that arise at this stage are the pressure on space in the various fields covered by Nature and the likelihood that the manuscript would seem of great topical interest to those working in the same or related areas of science. We believe that the arguments put forward have been well rehearsed in the past and would be better suited to an AIDS journal.
Sorry not to be more positive on this occasion.
Dr Richard Gallagher >Biological Sciences Editor
COMMENTARY: THE DURBAN DECLARATION
Eleni PapadopulosEleopulos (1), Valendar F.Turner (2), John M. Papadimitriou (3), David Causer (1), Barry Page (1), Helman Alfonso(4)
1) Department of Medical Physics, 2) Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia; 3) Department of Pathology, University of Western Australia; 4) Department of Research, Universidad Metropolitana Barranquilla, Colombia.
For the HIV theory of AIDS to be accepted, evidence must exist which proves:
(1) As stated in the Declaration, "Patients with acquired immune deficiency syndrome, regardless of where they live, are infected";
(2) The theory can account for all the phenomena for which it was put forward;
(3) Its predictions have been fulfilled .
Since by definition a patient is said to have AIDS only if he/she has a positive antibody test, the only test routinely used to prove HIV infection, it follows that all patients have a positive antibody test.
However, questions exist as to what the test means. In the antibody tests some proteins which are said to be HIV proteins are reacted with patient sera.
According to Luc Montagnier, the leader of the team that claimed to have discovered HIV seventeen years ago, the characterisation of proteins as HIV proteins "demands mass production and purification [of the virus], it is necessary to do that".1 Ten years before, the principal and second authors of Montagnier et al. 1983 paper also stressed that to characterise a retrovirus and its constituents one must purify the particles, that is, isolate them from any other biological constituents.2, 3
This has not been done either by Montagnier or anybody else, a fact accepted by some of the best known protagonists of the HIV theory.4, 5 In fact, in 1997, Montagnier acknowledged that the material which he and his colleagues claimed to be "purified" HIV did not even have particles with "the morphology typical of retroviruses".1 Nonetheless, because some proteins, including a protein of molecular weight 24,000 in this material reacted with patient sera, they chose to call these HIV proteins, and the antibodies, HIV antibodies.
At present there is ample evidence that the "HIV" proteins are cellular proteins4, 6-8 Evidence also exists that AIDS patients and those at risk have auto-antibodies as well as antibodies to a plethora of infectious agents which cross-react with the "HIV" proteins.6, 9, 10 In other words, whatever positive antibody test means it cannot be considered proof for HIV infection.
The fact that a positive antibody test does not mean HIV infection is accepted by the test kits’ manufacturers: "At present there is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood.11
The HIV theory of AIDS was put forward to account for the high frequency of some clinical and laboratory phenomena in Gay men, IV drug users, and haemophiliacs, none of which were new. The main clinical phenomena were Kaposi's sarcoma (KS) and Pneumocystis carinii pneumonia, the former constituting the basis for a relationship between AIDS and retroviruses. At present everybody, including the CDC, acknowledges that HIV plays no role, either directly or indirectly, in the development of KS.12, 13
The laboratory phenomenon was a decrease in T4 cells, determined by binding of the CD4 antibodies. It was postulated that HIV infection leads to T4 destruction (Acquired Immune Deficiency, AID), which in turn leads to opportunistic infections, S.
Thus, the foundation of the HIV theory is:
Infection with HIV --> T4 Destruction (AID) --> Syndrome (S). Step 1 Step 2 Step 3
Even if one assumes that the first step is proven, the theory cannot be accepted unless the other two are also proven.
At present there is evidence that the decrease of T4 cells in blood is not due to their destruction by HIV or any other factor, and that decrease in T4 cells is not correlated with disease progression.:
"This article discusses the importance of alterations in the CD4+ and CD8+ cell migration in regulating blood lymphocyte levels and questions the extent of virus-mediated CD4+ cell destruction";14
"CD4+ T-cell lymphopenia is due to both shortened survival time and a failure to increase the production of circulating CD4+ T-cells";15 or to the down-regulation of the CD4 molecule.16
In other studies it was shown that, "CD4 [T4] cell counts were not significantly associated with the risk of progression" to disease and that "Along with other recent analyses and experimental developments these conditions also suggest a need to re-evaluate current concepts about HIV pathogens including the concept that a systemic depletion of CD4 T-cells is the hallmark of the disease".17
In fact, evidence exists which shows that "low numbers of T4 cells was the highest risk factor for HIV infection", that is, decrease in T4 cells is the cause and not the effect of "HIV seroconversion".18 , 19 It may be of interest to note that as early as 1985, Montagnier knew that the immune deficiency in the AIDS risk groups was not caused by HIV: "This [AID] syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV [HIV] infection".20
In conclusion, a decrease in T4 cells is neither necessary nor sufficient for disease to develop. This finding totally contradicts the HIV theory of AIDS, that is, that HIV infection results in a decrease in T4 cells (AID) which in turn results in S (diseases), and by itself is sufficient for one to question the HIV theory of AIDS.
The main prediction of the HIV theory of AIDS was that, although AIDS was first diagnosed in Gay men, because AIDS was caused by a sexually transmitted agent which like all other such agents is bidirectionally transmitted, AIDS would rapidly spread throughout the heterosexual population.
One of the first scientists to publish data that this could not be the case, at least in Gay men, was Robert Gallo and his associates. In 1984 he wrote: "Of eight different sex acts, seropositivity correlated only with receptive anal intercourse...".21 In 1986 Gallo wrote: "Data from this and previous studies have shown that receptive rectal intercourse, for example, is an important risk factor for HTLV-III [HIV] infection...We found no evidence that other forms of sexual activity contributed to the risk".22
This was confirmed in many other studies, including the Multicenter AIDS Cohort Study, (MACS), the best, largest (about 5,000 men), and longest study which commenced in 1984 and is ongoing.23 In this, as well as other studies, it was shown that it is the frequency of passive anal passive intercourse, not the number of partners which is important in the development of a positive antibody test and AIDS.24-26
In a 1994 review of most, if not all the epidemiological studies conducted in Gay men, the authors concluded: "It can be said that the cited reports yield convincing evidence that (1) unprotected ano- genital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection; (2) ano-genital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection; (3) there is mounting epidemiological evidence for a small risk attached to oro-genital receptive sex, biologic plausibility, credible case reports and some studies show a modest risk, detectable only with powerful designs; (4) sexual practices involving the rectum and the presence of (ulcerative) STD facilitate the acquisition of HIV-1; (5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as ano-genital insertive intercourse and oro-anal sex...(8) the association of substance use with HIV infection is probably the result of interaction, because substance use increases the likelihood of practising ano- genital receptive intercourse".27
Unquestionably, to date, the best designed and executed study in heterosexuals was conducted by Nancy Padian and her associates. In 1987 they reported: "The total number of exposure to the index case (sexual contacts with ejaculation) and the specific practice of anal intercourse" were associated with the development of a positive antibody test. The results from their long (ten years) prospective study of heterosexual couples of whom only one partner of either sex was antibody positive were published in 1997 where they reported that "no seroconversions occurred among exposed partners".28
According to one of the best known HIV/AIDS experts, Jaap Goudsmit, for heterosexual "HIV transmission" anywhere in the world, including Haiti, Africa, Thailand, "a homosexual or anal factor seems to be required".26 In other words, at present there is ample evidence that sex plays an important role in the acquisition of a positive antibody test and AIDS and the practice of safe sex should form the basis for any effort in prevention.
However, there is no proof that AIDS is a bidirectionally sexually transmitted disease. Unlike any other sexually transmitted disease, AIDS and a positive antibody test, like pregnancy, can be sexually acquired but not sexually transmitted. The difference is that while pregnancy can be acquired by a single sexual intercourse, for AIDS to appear a very high frequency of receptive anal intercourse over a long period is necessary. AIDS is more like anal29, 30 and cervical cancer.31 The effect is not the result of the act itself but its high frequency.
However, as with pregnancy, cervical and anal cancer, other factors may promote or militate against the development of AIDS and a positive antibody test.
If a hypothesis cannot account for the phenomena for which was put forward, and if its predictions are not fulfilled, then scientists have no choice but to reappraise it.
1. Tahi, D. Continuum 5, 30-34 (1998). 2. Toplin, I. Spectra , 225-235 (1973). 3. Sinoussi, F., Mendiola, L. & Chermann, J.C. Spectra 4, 237-243 (1973). 4. Bess, J.W., Gorelick, R.J., Bosche, W.J., Henderson, L.E. & Arthur, L.O. Virol. 230, 134-144 (1997). 5. Gluschankof, P., Mondor, I., Gelderblom, H.R. & Sattentau, Q.J. Virol. 230, 125-133 (1997). 6. Papadopulos-Eleopulos, E., Turner, V.F. & Papadimitriou, J.M. Bio/Technology 11, 696-707 (1993). 7. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. & Causer, D. Continuum 4, 1s-24s (1996). 8. Arthur, L.O., et al. J. Virol. 69, 3117-24 (1995). 9. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M. & Causer, D. Curr. Med. Res. Opinion 13, 627-634 (1997). 10. Papadopulos-Eleopulos, E., Turner, V.F., Papadimitriou, J.M., Causer, D. & Page, B. Curr. Med. Res. Opinion 14, 185-186 (1998). 11. Abbott Axsym system (HIV-1/HIV-2). Abbott Laboratories, Diagnostics Division, Abbott Park. Illinois: United States of America, 1988. 12. Beral, V., Peterman, T.A., Berkelman, R.L. & Jaffe, H.W. Lancet 335, 123-128 (1990). 13. Redfield, R.R. & Burke, D.S. Sci. Am. 259, 70-78 (1988). 14. Rosenberg, Y.J., Anderson, A.O. & Pabst, R. Immunol. Today 19, 10-7 (1998). 15. Hellerstein, M., et al. Nat. Med. 5, 83-89 (1999). 16. Marodon, G., Warren, D., Filomio, M.C. & Posnett, D.N. Proc. Nat. Acad. Sci. U S A 96, 11958-63 (1999). 17. Katzenstein, D.A., et al. NEJM 335, 1091-8 (1996). 18. Des Jarlais, D.C., et al. J. Acquir. Immun. Defic. Syndr. 6, 820-822 (1993). 19. Nicolosi, A., et al. Epidemiology 1, 453-459 (1990). 20. Montagnier, L. Ann. Int. Med. 103, 689-693 (1985). 21. Goedert, J.J., et al. Lancet 2, 711-6 (1984). 22. Stevens, C.E., et al. JAMA 255, 2167-2172 (1986). 23. Kingsley, L.A., et al. Lancet i, 345-348 (1987). 24. Moss, A.R., et al. Am. J. Epidemiol. 125, 1035-47 (1987). 25. Palenicek, J., et al. J Acquir Immune Defic Syndr 5, 1204-11 (1992). 26. Goudsmit, G. Viral Sex-The Nature of AIDS (Oxford University Press, New York, 1997). 27. Caceres, C.F. & van Griensven, G.J.P. AIDS 8, 1051-1061 (1994). 28. Padian, N.S., Shiboski, S.C., Glass, S.O. & Vittinghoff, E. Am. J. Epidemiol. 146, 350-357 (1997). 29. Daling, J.R., et al. NEJM 317, 973-7 (1987). 30. Kondlapoodi, P. JAMA 248, 2114-5 (1982). 31. Reid, B.L., French, P.W., Singer, A., Hagan, B.E. & Coppleson, M. Lancet 2, 60-2 (1978).
-- Mark Gabrish Conlan (email@example.com), March 09, 2001.