Host restriction of HIV-1 by APOBEC3 and viral evasion through Vif.
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.
Niewiadomska
Anna Maria
AM
Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Yu
Xiao-Fang
XF
D000071478:APOBEC Deaminases; D000163:Acquired Immunodeficiency Syndrome / Q000517:prevention & control*; D002453:Cell Cycle; D003564:Cytidine Deaminase; D043525:Cytosine Deaminase / Q000502:physiology*; D015497:HIV-1; D006801:Humans; D057131:Immune Evasion; D046988:Proteasome Endopeptidase Complex / Q000502:physiology; D054320:vif Gene Products, Human Immunodeficiency Virus / Q000502:physiology*
D054320:vif Gene Products, Human Immunodeficiency Virus; C514847:vif protein, Human immunodeficiency virus 1; D046988:Proteasome Endopeptidase Complex; D043525:Cytosine Deaminase; D000071478:APOBEC Deaminases; C502889:APOBEC3 proteins, human; D003564:Cytidine Deaminase