14th Conference on Retroviruses and Opportunistic Infections Los Angeles, California - February 25-28, 2007

Conf Retrovir Opportunistic Infect 2007 Feb 25-28;14: (abstract no. 49)

Tariq Rana
Univ of Massachusetts Med Sch, Worcester, US

BACKGROUND: Successful replication of viruses and other intracellular pathogens in their respective host cells requires that they overcome a series of replication restrictions or “roadblocks” established by the cell. In the case of HIV-1, the ability of the virus to replicate in human cells is dependent on its ability to neutralize APOBEC3G, a DNA editing enzyme that incorporates into virions and renders them noninfectious. Although a potentially devastating inhibitor of HIV-1 replication, the virus evades APOBEC3G by inducing its degradation during virus assembly. APOBEC3G is also capable of inhibiting the replication of other retroviruses as well as the hepadnavirus hepatitis B, a DNA virus that replicates through an RNA intermediate, suggesting that APOBEC3G may function in cellular defense against a broad range of viral pathogens.

CONCLUSIONS: Our recent findings showing that APOBEC3G localizes to specialized compartments in the cytoplasm of mammalian cells known as mRNA processing (P) bodies, which function in the degradation and storage of cellular mRNA, will be presented. Implications for APOBEC3G function and for the role of P-bodies in both cellular defense against viruses and retroviral assembly will be discussed.

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2007-02-25
49

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