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Target Of AIDS Virus Identified, Boosting Hope For Drug With PM-AIDS Commission, Bjt

June 3, 1988

PASADENA, Calif. (AP) _ A powerful ″second-generation″ anti-AIDS drug could be available within a decade, say scientists who helped identify the precise target where the AIDS virus latches onto cells it destroys.

The study by scientists at the California Institute of Technology here, Ortho Pharmaceuticals in Raritan, N.J., and the University of Alabama, Birmingham was published today in the journal Science.

The study’s chief authors, Caltech molecular biologist Bradford Jameson and protein chemist Stephen B.H. Kent discouraged excess optimism that their discovery would lead to a drug to treat or cure acquired immune deficiency syndrome, which cripples the body’s disease-fighting immune system.

″We do not want to give people false hope,″ said Kent. Nonetheless, he said, a drug more effective than those now being developed could be available in 10 years.

However, Dr. Mathilde Krim, a founder of the American Foundation for AIDS Research, said Kent was exaggerating the time it would take to develop a drug using the new discovery.

″If things go very well, I’d say two years until it would be made available to people,″ Krim, whose organization funded the $120,000 study, said by phone from New York City.

″To my knowledge, it is the first time a binding site has been identified with such precision for any virus,″ Krim said. ″It’s a wonderful accomplishment.″

Scientists previously knew the AIDS virus infects T4 white blood cells and certain other cells by attaching to CD4, a ″receptor″ protein on the cells’ surface. T4 cells are the main immune-system cells destroyed by AIDS.

Using sophisticated analyses, Jameson identified the exact part of the CD4 protein to which the AIDS virus attaches, known as a ″binding site.″

In the next step, crude synthetic copies of the binding site were manufactured by Jameson, Kent and Caltech biology chairman Leroy Hood.

Alabama scientists found that in the test tube, the fake binding sites acted as decoys to overwhelm AIDS virus particles so they couldn’t latch onto real binding sites on T4 cells.

If scientists can create more sophisticated versions of the fake binding site, those might work as a drug to treat or cure AIDS, or to carry virus- killing drugs to the AIDS virus, Kent said.

″This is the first step toward a second-generation drug,″ he said.

The finding ″should provide information that will guide future efforts to develop agents capable of blocking the virus,″ agreed Dan Capon, a molecular biologist at Genentech Inc., a South San Francisco company using a similar approach to develop anti-AIDS drugs.

Kent and Jameson said their findings are important in learning how viruses infect cells, and might be use to create drugs to fight other viruses and treat rheumatoid arthritis and other autoimmune diseases, in which the body is attacked by its own immune system. Such drugs could also prevent the immune system from rejecting transplanted organs.

A major obstacle is that either fake CD4 proteins or fake binding sites might also prevent the immune system from doing its job, Kent said.

However, Krim said that risk should be much lower if fake binding sites rather than fake CD4 proteins are used in a drug, and that such risk would be acceptable in treating severely ill AIDS patients.

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