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

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

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.

Publication types

  • Review

MeSH terms

  • APOBEC Deaminases
  • Acquired Immunodeficiency Syndrome / prevention & control*
  • Cell Cycle
  • Cytidine Deaminase
  • Cytosine Deaminase / physiology*
  • HIV-1*
  • Humans
  • Immune Evasion
  • Proteasome Endopeptidase Complex / physiology
  • vif Gene Products, Human Immunodeficiency Virus / physiology*

Substances

  • vif Gene Products, Human Immunodeficiency Virus
  • vif protein, Human immunodeficiency virus 1
  • Proteasome Endopeptidase Complex
  • Cytosine Deaminase
  • APOBEC Deaminases
  • APOBEC3 proteins, human
  • Cytidine Deaminase