U of A Researchers find potential HIV treatment

Discovery helps make significant advances in HIV research-Barr

Logan Banadyga, News Writer Tuesday, 4 March 2008

Scientists at the University of Alberta have uncovered a human gene that stops the spread of HIV, potentially opening the door to new treatments in the battle against AIDS.

The team of researchers, led by molecular virologist Dr Stephen Barr, a post-doctoral fellow in the Department of Medical Microbiology and Immunology, first identified the gene—known as TRIM22—as a possible antiviral protein three years ago.

TRIM22 is one of hundreds of genes turned on by interferons, chemicals produced by our immune system to combat viral infections.

“It’s been known for a long time that interferon treatment of cells can block HIV infection, but nobody really knew how or what the genes were that were involved,” Barr explained.

“We found that TRIM22 was turned on quite a bit in response to interferons [...], and our later studies showed that [it] actually blocked [HIV] by trapping the virus within cells so it can’t get out to infect other cells.”

According to Barr’s study, published last week in the journal Public Library of Science Pathogens, TRIM22 interacts with the major protein that is required for HIV assembly, and this interaction, Barr said, somehow blocks the assembly of the virus.

“These results are very exciting [...] because they show that our bodies have a gene that is capable of stopping the spread of HIV,” he explained.

Although HIV replication can be blocked at earlier stages in the virus’ life-cycle, this is the first time that an antiviral protein has been shown to interfere specifically with the later stage of HIV assembly. The unique activity of TRIM22, Barr explained, identifies a new strategy for treating HIV infection.

“The goal would be to basically harness this antiviral activity,” he said, noting that the ultimate, but long-term, goal of his research is the development of new drugs and vaccines capable of halting the spread of HIV and the onset of AIDS.

“If we can find ways to slow the release of virus so that it can’t infect other cells, that has the potential of slowing or preventing the onset of AIDS in patients,” he continued.

Dr James Smiley, a Canada Research Chair in Molecular Virology and a professor at the U of A who operates the lab in which Barr worked, is enthusiastic about the impact these findings will have on the HIV field and what they will mean for the University’s reputation.

“These types of discoveries help to solidify and enhance the U of A’s profile in the area of infection and immunity,” Smiley said, adding that “the U of A provides an environment where talented post-doctoral fellows such as Steve Barr can pursue their research in any area that they choose.”

Barr, who began his work in Smiley’s lab over two years ago, will next turn his attention to what he says are the two major outstanding questions from his research: how exactly TRIM22 interferes with HIV assembly and why this gene doesn’t appear to work in people infected with HIV.

With approximately 33 million people worldwide reported to be living with HIV and 2 million deaths caused each year by HIV/AIDS, Barr expects that his research will provide hope to those living with the so-far-incurable disease.
With emerging drug-resistant strains and failed vaccine trials, Barr said, “there’s been a real dark cloud put over HIV research fairly recently.” However, he added that “we are making significant advances.”