The virus that causes AIDS commandeers a white blood cell?s own inner machinery?producing more virus particles to invade new cells, 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. Based on the research, Myriad Genetics is working to develop such a drug, he said.
Because strains of HIV resistant to current AIDS treatments have sprung up recently, drugs which use different mechanisms to thwart the virus must be developed.
The doctors need the ?next generation? drugs to fight increasing resistance in both bacterial and viral infections.
?It?s a constant war,? Sundquist said.
HIV, the virus responsible for AIDS, enters a host cell. Acting like a parasite, it causes the cell to produce thousands of copies of the virus? genetic code. New viral particles collect at the cell?s membrane?ready to be released, according to Sundquist.
The authors found when a certain cellular protein was eliminated, the viral particles could not bud off and leave the cell. Instead they remained stuck at the cell?s surface, unable to spread the infection.
They determined the protein binds to the viral particle and initiates the budding process. The protein is a crucial part of a pathway that probably involves many proteins, Sundquist said.
In a healthy cell, this pathway is involved in transporting materials for degradation, all 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 eventually destroys.
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 they determined the function of the protein, tests with the actual HIV began.
The gene responsible for producing the cellular protein was inactivate so the host cell could not produce the protein. A virus invading this 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.