AIDS Virus Studied By U Researchers

The virus that causes AIDS commandeers a white blood cell?s own inner machinery?producing more virus particles to invade new cells thus spreading the disease.

But researchers at the University of Utah and Myriad Genetics in Research Park have found a key component to a viral particle?s escape from its host cell.

Their results will appear in the Oct. 5 issue of the journal Cell.

This is still ?basic research? according to Wes Sundquist, an author of the study and a professor of biochemistry.

However, the discovery does have the potential to yield a drug treatment for AIDS, the disease resulting from infection by the HIV virus. Based on the research, Myriad Genetics is working to develop such a drug, he said.

Because strains of HIV resistant to current AIDS treatments are appearing, researchers must develop drugs that use different mechanisms to thwart the virus.

Their discovery could form the basis for a drug to reduce the amount of HIV in an infected person. Like treatments on the market now, it would make the disease more livable?not cure it.

Increasing resistance among both bacterial and viral infections, like AIDS, demands the ?next generation? of drugs.

?It?s a constant war,? Sundquist said.

HIV enters a host cell, and, acting like a parasite, it causes the cell to produce copies of its own genetic code. New viral particles collect at the cell?s membrane?ready to be released, according to Sundquist.

The authors found when they eliminated a certain cellular protein, the viral particles could not bud off and leave the cell. Instead, the particles remained stuck at the cell?s surface, unable to spread the infection.

The researchers determined the protein binds to the viral particle and initiates the budding process, which releases it from the infected cell. The protein is a crucial part of a pathway that probably involves many other proteins, according to Sundquist.

In a healthy cell, this pathway is involved in transporting materials for degradation within the cell.

Though scientists already knew about the existence of the protein, the study uncovered the crucial role it played in the virus? escape from the host cell it will eventually destroy.

Their discovery may influence research into treatments of diseases other than AIDS.

?We think the pathway is likely to affect other viruses,? Sundquist said.

Myriad Genetics did the initial ?fishing expedition,? according to Uta von Schwedler, a postdoctoral fellow and an author of the paper.

Once the authors determined the function of the protein, tests with the actual HIV began.

Researchers inactivated the gene responsible for producing the cellular protein. The host cell was then unable to produce the protein. It turned out that a virus-invading sort of host cell could not be infectious, von Schwedler said.

The U keeps HIV samples in a secured facility. Only three people have access to the virus, she said. Inside, they must put on gloves, goggles and other protective wear.

The only sorts of diseases afforded more care are airborne ones, like Ebola. The U does not keep diseases this dangerous, she said.

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