AIDS in the 1990s: More Questions than Answers

by Colman Jones

As scientists prepare for yet another AIDS conference, the outlook remains unremittingly bleak. Despite billions of dollars worth of research over the last decade, a cure or preventive vaccine for AIDS remains out of reach. This impasse, coupled with a rising infection rate in the Third World, have led both medical researchers and AIDS activists to become increasingly frustrated with the pace of scientific progress against this killer.

Complicating the research effort are nagging unanswered questions: it remains unclear how HIV, the virus most scientists believe causes AIDS, destroys the immune system. There’s no consistent strain that’s always associated with the disease. Powerful anti- HIV treatments, such as AZT, are disappointing failures.

Even Luc Montagnier, the French scientist whose team originally discovered HIV, no longer believes the virus is sufficient to bring on the disease by itself, and has long called for research into possible “co-factors”. Indeed, the rate at which different groups of HIV-positive people develop AIDS, and the astonishing diversity of symptoms, suggest that something more than HIV is at work.

Recent findings by immunologists at the National Institutes of Health seem to indicate that HIV can be harmless under certain conditions. They have identified many people whose immune systems have unquestionably been exposed to, and even infected by the virus, but who do not make HIV antibodies or get sick. By measuring the response of key immune cells, known as T-cells, the NIH researchers have discovered that a surprising large number of these poeple who have HIV – but test negative for HIV antibodies – have been able to control the virus through a strong response by the cellular arm of their immune system.

The NIH researchers believe the activation of HIV out of latency may reflect a fundamental shift in the immune system itself, from a response in which T-cells work to control infection, to a response in which antibodies predominate. Such a deviation in the immune response is increasingly recognized as the mechanism behind not only HIV activation, but also why a host of other bacterial diseases can become chronic, while others are successfully resolved. The problem seems to stem from immune responses being shut off too early. They’re tricked into leaving behind a few residual organisms that then slowly multiply, and give rise to persistent infection. Chronic diseases that work in this fashion include tuberculosis, leprosy, sleeping sickness, and syphilis.

In fact, some people feel that AIDS should be renamed “Acquired Immune Deviation Syndrome”, in which certain cells start sending inappropriate levels of chemical signals (known as “cytokines”) to each other. This eventually burns out the immune system. It’s conceivable that many “co-factors” can alter the immune system in this way – cytokine poisoning of blood products, chronic opiate abuse, tropical diseases in Africa, to name just a few.

“There are many ways to get AIDS, and there always have been”, says John Scythes, a Toronto investigator who has published his views at previous AIDS and STD conferences. A former plumber, and now bookseller, Scythes is a unique breed of lay scientist, convinced that unresolved syphilis is at the heart of sexually- acquired AIDS, owing to the profoundly deviating effect syphilis has on the immune system. He has been repeatedly invited to lecture on the topic at European universities, although most North American researchers ignore him.

To back up his concerns, Scythes points to numerous epidemiologic studies showing that a history of syphilis is one of the best predictors of subsequently turning HIV-positive. A study of 500 gay men in Amsterdam showed that while those who had unprotected receptive anal sex and/or multiple partners were roughly twice as likely to seroconvert, i.e. turn “HIV-positive”, as those who didn’t, those with a history of syphilis were over 20 times as likely to be HIV-positive than those without a history of syphilis. A large U.S. Army study had similar findings.

Yet, despite this overwhelming association, the classical forms of late syphilis are virtually non-existent among people with AIDS. But these tertiary symptoms, a distinct and easily recognizable set of allergic-like, inflammatory reactions involving tissue destruction, are actually the result of a vigorous cellular response, in which the body’s cells are sensitized, or primed, against the organism.

Some researchers feel that the absence of typical symptoms doesn’t necessarily mean that an underlying syphilis infection is harmless. They concede it’s entirely possible that in people who become de-sensitized–i.e., whose immune systems have grown tolerant to syphilis–the disease can cause the kind of chronic immune deviation that might very well lead to AIDS, without producing any of the typical symptoms of late syphilis.Pencillin alone would have very little effect in such people whose immune systems were no longer sensitized to the syphilis organisms.

Additionally, the reliability of the blood tests used to detect syphilis in people with HIV is coming under increasing scrutiny. Disturbing anomalies in test results – including a mysterious and highly selective disappearence of normally lifelong antibodies to syphilis – have been uncovered over the last few years by various centres around the world, including the Ontario health ministry’s Laboratory Services Branch.

But research directed at a possible AIDS-syphilis connection has been slow in coming. The medical community is dominated by HIV-related research and funding, with few resources available for other strategies.

As Dr. Sandra Larsen, a syphilis expert at the U.S. Centers for Disease Control, put it, “We have not looked at some of these concerns, because we just haven’t had the funding, nor the time, nor the means for doing it. We have a limited budget, and a limited number of people, and we’re shrinking daily.”

Why is it so hard to get funding? “Well,” says Larsen, “people feel that syphilis can be controlled with penicillin. I mean, you have to realistic: syphilis is not in the favored populations.”

In the meantime, Scythes is doing what he can to help the research along. Scythes recently paid $500 to have antibodies that count rabbit T-cells shipped to Budapest, so that Hungarian syphilis expert Istvan Horvath can analyze the immune systems of a series of syphilitic rabbits, who appear to be suffering from an AIDS-like syndrome. As millions of dollars continue to be spent in the U.S. on HIV research, it would be ironic indeed if an answer to sexually-transmitted AIDS came out of a collaboration between a lab in Budapest and a former plumber.

Colman Jones is a freelance journalist based in Toronto.

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