Researcher Helps Discover A Way To Prevent The HIV Ability To Mutate

February 19, 2009 at 11:00 am Leave a comment

Trying to stop HIV early in its life cycle by preventing the virus from entering the body’s cells and fusing is the job of drugs called fusion inhibitors. Currently, the last line of defense – the drug T20 – eventually fails as the virus mutates. A new study from researchers at the University of Missouri and Kyoto University in Japan shows that a modification to T20 can deliver a preemptive strike to the virus’ ability to replicate. This new finding could give patients more options to stay healthy for a longer period of time.

“Fighting HIV is a catch-up game,” said Stefan Sarafianos, PhD, assistant professor of microbiology and immunology in the MU School of Medicine and Bond Life Sciences Center. “We constantly try to improve the drugs because the virus tries to replicate on a continuous basis. This new study shows that we may have found the next generation fusion inhibitor.”

Early in the life cycle of HIV, the virus tries to enter a host cell in the body and fuse with the cell in order to start replicating, integrating into the DNA and maturing into AIDS.

There are two common mutations that are multi-drug resistant strains. The mutations help the virus escape, but with a reduced ability to replicate. Eventually it evolves into a second mutation that allows the virus to replicate at its original ability. This is the point where current drugs fail to keep the virus out of the body’s cells. In this new study, the modified T20 recognized the double mutations and started blocking these strains as well.

“This variant of T20 will provide more options for resistance,” Sarafianos said. “This stage in the HIV life cycle provides a huge opportunity for intervention. We try to think ahead about what the virus is going to do and design something that not only helps with what is currently happening in the body but also prevents what might occur in the future.”

The study will be featured on the cover of the Feb. 20 issue of The Journal of Biological Chemistry. It was done in collaboration with researchers from the Institute for Virus Research at Kyoto University in Japan.



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