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Curr Top Microbiol Immunol. 2009;339:1-25. doi: 10.1007/978-3-642-02175-6_1.

Host restriction of HIV-1 by APOBEC3 and viral evasion through Vif.

Author information

1
Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.

Abstract

The arms race between virus and host is a constant battle. APOBEC3 proteins are known to be potent innate cellular defenses against both endogenous retroelements and diverse retroviruses. However, retroviruses have developed their own methods to launch counter-strikes. Most primate lentiviruses encode a protein called the viral infectivity factor (Vif). Vif induces targeted destruction of APOBEC3 proteins by hijacking the cellular ubiquitin-proteasome pathway. Here we review the research that led up to the identification of A3G, the mechanisms by which APOBEC3 proteins can inhibit retroelements, and the counter-mechanisms that HIV-1 Vif has developed to evade its antiviral activities.

PMID:
20012521
DOI:
10.1007/978-3-642-02175-6_1
[Indexed for MEDLINE]

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