| Literature DB >> 20702647 |
Angelo Kolokithas1, Kyle Rosenke, Frank Malik, Duncan Hendrick, Lukas Swanson, Mario L Santiago, John L Portis, Kim J Hasenkrug, Leonard H Evans.
Abstract
APOBEC proteins have evolved as innate defenses against retroviral infections. Human immunodeficiency virus (HIV) encodes the Vif protein to evade human APOBEC3G; however, mouse retroviruses do not encode a Vif homologue, and it has not been understood how they evade mouse APOBEC3. We report here a murine leukemia virus (MuLV) that utilizes its glycosylated Gag protein (gGag) to evade APOBEC3. gGag is critical for infection of in vitro cell lines in the presence of APOBEC3. Furthermore, a gGag-deficient virus restricted for replication in wild-type mice replicates efficiently in APOBEC3 knockout mice, implying a novel role of gGag in circumventing the action of APOBEC3 in vivo.Entities:
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Year: 2010 PMID： 20702647 PMCID： PMC2950561 DOI： 10.1128/JVI.01023-10
Source DB: PubMed Journal: J Virol ISSN： 0022-538X Impact factor: 5.103