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An update on the search for a vaccine to fight AIDS. Fred De Sam Lazaro of public station KTCA-St. Paul-Minneapolis, reports.

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FRED DE SAM LAZARO: In the hunt for a vaccine against HIV, scientists have found some of their earliest leads on the African continent. Last year, the NewsHour reported on a study of prostitutes in Panmwania, a crowded slum just outside Kenya's capital, Nairobi. For 15 years, a team of Canadian and Kenyan doctors has studied about 2,000 women who visit this clinic for outpatient care. Almost all of the women eke out a living as prostitutes, and almost all of them have tested positive for the AIDS virus. It's the remaining 5 percent or so--patients like Joyce Wanjiro--who began to intrigue the doctors some years ago.

JOYCE WANJIRO: (speaking through interpreter) I don't know why I am not getting it, because I have been in the business for a long time. Many of my friends have it. Some have died.

FRED DE SAM LAZARO: Wanjiro has remained HIV-negative, despite repeated exposure for years to the virus. Dr. Frank Plummer of the University of Manitoba is the study's chief scientist.

DR. FRANK PLUMMER, University of Manitoba: I'm thinking more and more that these women represent an instance of natural immunity to HIV, and that if we can understand that, what's mediating it, why it occurs,,then I think there's a good chance that we can duplicate that artificially and make a vaccine.

FRED DE SAM LAZARO: Plummer's theory is that his HIV-resistant subjects have a rare type of HLA genes. These are molecules on immune cells, and Plummer says in the case of these women, they may be repelling the virus. There are other theories or approaches to studying this phenomenon of natural resistance. In May, a team at the National Institutes of Allergic & Infectious Diseases identified a type of molecule that had been hunted for years. It plays a key role in the infection of T-cells, a type of white blood cell in the immune system.

DR. ED BERGER, National Institutes of Health: We've known for about a dozen years now that the first step in which the HIV virus infects a cell is that the HIV virus attaches to a certain molecule on the surface of the cell called CD-4.

FRED DE SAM LAZARO: But there's a crucial second step that requires another receptor molecule besides CD-4. Dr. Ed Berger's team identified this cofactor after an exhaustive search through libraries of human genes. They named it Fusin, after its chief function.

DR. ED BERGER: In order for the virus to inject its genetic material into the cell, there has to be a fusion of them between this membrane and this membrane. These are like two soap bubbles, and this membrane has to fuse with that membrane in order for this genetic material to get into the cell. So we knew that CD-4 is not enough for that to happen. It's something else on this cell is required. So the discovery that we made is that we discovered a particular molecule on the surface of this cell that allows this fusion of them to occur. And that's a molecule that we've given the name Fusin because it allows the fusion between these two membranes.

FRED DE SAM LAZARO: Once the virus fuses or integrates genetically with the host cell, it triggers a breakdown in the immune system, leading to AIDS. So logically, Berger and others speculate that a person's Fusin status could determine response to HIV.

DR. ED BERGER: Perhaps some individuals are defective in either the production of Fusin, or the Fusin molecule may be a little bit different, so that the HIV virus that uses Fusin cannot get into cells. There's a great deal of interest in testing whether those individuals might be either missing those cofactors, or the cofactors may be genetically altered in such a way that the virus can't use them.

FRED DE SAM LAZARO: A plausible theory, but it turns out not applicable to the Kenyan subjects. Dr. Plummer says something else is protecting them from HIV.

DR. FRANK PLUMMER: We don't think that this is important in this phenomena because we can very readily infect these women's T-cells with viruses that prefer to grow in T-cells. This is not to say that some other coreceptor that we don't yet know about isn't involved, and that could well be.

FRED DE SAM LAZARO: Last fall, several teams of scientists identified another cofactor, a gene called CKR-5. CKR-5 is found primarily in cells that are infected during sexual transmission of HIV. Further investigation of the CKR-5 gene revealed that it is mutated or altered in about one out of five people, with startling benefits. In studying blood samples from people repeatedly opposed to HIV, hemophiliacs, IV drug users, some gay males, scientists found those with the mutated CKR-5 were either immune to HIV, or survived with the infection for many years with no related health problems. But, alas, when scientists searched for the CKR-5 mutation among the Kenyan prostitutes, they failed to find it in a single patient.

DR. FRANK PLUMMER: So the CKR-5 receptor story doesn't seem to be involved in this phenomena of resistance that we're seeing. It's very important in Caucasian populations probably. Now, that doesn't mean another receptor couldn't be involved in the situation in Panmwania.

FRED DE SAM LAZARO: Plummer and other researchers hope to track down corresponding receptors in African populations. It's a daunting task. There could be dozens of receptors or co-factors. Add to that complication of virus that's a moving target constantly mutating so it can outfox the immune system.

DR. FRANK PLUMMER: We're trying to build a jigsaw puzzle without knowing what the whole puzzle looks like.

FRED DE SAM LAZARO: Distant as any vaccine seems, researchers say the discovery of receptors like Fusin and CKR-5 may now allow scientists to infect small laboratory animals with HIV, a major advancement in testing potential vaccines or drugs.

DR. ED BERGER: The problem with animal models for HIV is that they don't have the necessary molecules for HIV to get into the cells, so with the identification of Fusin, we're very optimistic that if we put into an animal the gene for CD-4, as well as the gene for Fusin, that now we'll have a good animal model that could be infected with HIV.

FRED DE SAM LAZARO: Although such predictions are extremely difficult, Plummer and Kenyan colleague Unzula Umu say based on the stepped up pace of recent discoveries, they may be able to launch a vaccine trial in three to five years.

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