ment of a new class of drugs to fight HIV infection-an entirely new approach in the anti-HIV arsenal, Greene said. Current drugs, such as reverse transcriptase and protease inhibitors, stop key viral protein enzymes from catalyzing reactions necessary to maintain the HIV viral life cycle. But scientists are coming close to exhausting the number of viral protein enzymes as potential drug targets. Greene and his research team are among the first to focus on non-enzymatic viral proteins, such as Nef, which interact with host cell proteins that HIV needs for its own growth.

Strong support for developing drugs that specifically target Nef comes from the observation that people infected with HIV strains lacking the nef gene-a rarity-develop AIDS symptoms much more slowly than those infected with HIV strains containing the nef gene.

"If we can win the battle at the single cell level, then we will be in a better position to win the war in the millions of HIV infected patients," Greene said.

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Contact: Laura Lane
llane@gladstone.ucsf.edu
415-476-2557
University of California - San Francisco
10-Apr-2001

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