United Press International - October 4, 2001
Bruce Sylvester from West Palm Beach, Fla.

"A virus cannot spread -- or 'bud' as we say -- without the help of a protein," said Wes Sundquist, lead investigator and professor of biochemistry at the University of Utah in Salt Lake City. "We found out that HIV distorts the workings of cellular proteins, and specifically the Tag101 protein, in order to do its dirty work.

"So a protein that normally helps keep a healthy cell alive and well becomes key to the way that the HIV virus spreads," he told United Press International.

Tsg101 and the other proteins identified in the study target other proteins within a cell for normal destruction and ejection -- the budding. As part of the process, Tsg101 and the other proteins make particles out of cell membrane material. The disposable material normally is put into those particles to be "budded" outward from the cell.

HIV overwhelms this process of cellular hygiene and uses it instead to spread the virus.

"In order to produce infectious virus, HIV uses the human cell machinery," said Adrian Hobden, president of Myriad Pharmaceuticals. "Understanding the appropriation of cellular machinery by the HIV virus should provide us with the means to disrupt the HIV lifecycle through therapeutic intervention."

The joint University of Utah-Myriad research is in the Oct. 5 issue of the journal Cell.

Myriad Genetics researchers also identified other proteins working with Tsg101 to allow viruses to bud and infect other cells.

Kenton Zavitz, a molecular biologist at Myriad, said these proteins will become research targets for potential new medicines.

"Current drugs on the market to fight AIDS are resulting in the emergence of drug-resistant mutants of HIV," Zavitz said. "Therefore, it is necessary to identify targets for new drugs that will be the next generation of antiviral medicines."

Scott Morham, another Myriad molecular biologist, suggested new drugs emerging from this research might help limit viral loads -- the amount of HIV -- in AIDS patients and in infected people who do have full-blown AIDS.

"This is still very basic science we are doing," Sundquist told UPI. "So we have to be careful about saying that any new therapy is around the corner. But, of course, we always hope that this kind of research will lead to positive developments on the therapeutic front. We are several years away at least from that kind of development out this work"

Stephen Goff, professor of biochemistry and molecular biophysics at Columbia University in New York, said another important event in the study was that researchers "used genetic technology to enter the cell turn off a protein, in this case Tsg101, to see what happens."

"Here it stopped the budding process and that stopped the spread of HIV to other cells," Goff told UPI. "That is hugely important."

He said this mechanism needs much more study to determine its importance to microbiologists.

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