Global view of how hiv/aids hijacks cells during infection

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Global view of how hiv/aids hijacks cells during infection

Global View of How HIV/AIDS Hijacks Cells During Infection


Gladstone Institutes scientist Nevan Krogan, PhD, has identified how HIV -- the virus that causes AIDS -- hijacks the body's own defenses to promote infection. This discovery could one day help curb the spread of the HIV/AIDS pandemic.


"One of the keys to HIV's success is how quickly it can evolve new attack strategies -- and the way in which it uses our own proteins against us is a prime example of that," said Dr. Krogan. "However, now that we've shed light on this complex process, we are one step closer to developing new drugs that will help us pull ahead in this evolutionary arms race."


AIDS has killed more than 25 million people around the world since first being identified some 30 years ago. In the United States alone, more than one million people live with HIV/AIDS at an annual cost of $34 billion. Dr. Krogan's experiments show promise for the development of more effective antiretroviral therapies for people with HIV. Further, they have laid the foundation for future research at Gladstone.


In his experiments, Dr. Krogan performed a two-part investigation of protein interactions. First, he conducted a systematic, global analysis of all potential interactions that occur between proteins made by the body (human proteins) and proteins made by the virus (HIV proteins). Second, he whittled down these ~500 interactions to the one that appeared most likely to fuel HIV infection: the interaction between the human protein CBFβ and the HIV protein Vif.


Normally during HIV infection, a restriction factor called APOBEC3G acts as a molecular roadblock, preventing the virus from reaching its target -- the CD4 T white blood cells that are a major component of the immune system. But Dr. Krogan found that when the HIV protein Vif binds to the human protein CBFβ, Vif is strengthened and APOBEC3G degrades. This degradation weakens ABOBEC3G's ability to stop HIV and the virus is free to infect the CD4 T cells.


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Bron: artikelvan Gladstone Institutes
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