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A conflict of interest: the evolutionary arms race between mammalian APOBEC3 and lentiviral Vif

Yusuke Nakano1, Hirofumi Aso1,2, Andrew Soper1

  • 1Laboratory of Systems Virology, Department of Biosystems Science, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoinkawara-cho, Sakyo-ku, Kyoto, 6068507, Japan.

Retrovirology
|May 10, 2017
PubMed

Insights

Mammalian APOBEC3 proteins fight lentiviruses, but lentiviruses use Vif proteins to degrade them. This ongoing battle between host APOBEC3 and viral Vif drives an evolutionary arms race.

Area of Science:

  • Virology
  • Evolutionary Biology
  • Immunology

Background:

  • Mammalian APOBEC3 proteins are cellular deaminases that inhibit lentivirus replication.
  • Lentiviruses encode the viral infectivity factor (Vif) protein to counteract APOBEC3 activity.
  • APOBEC3 proteins induce G-to-A hypermutations in the viral genome, while Vif targets APOBEC3 for degradation.

Purpose of the Study:

  • To review the co-evolutionary dynamics between mammalian APOBEC3 proteins and lentiviral Vif.
  • To summarize the current understanding of the host-virus interface driven by APOBEC3-Vif interactions.

Main Methods:

  • This review synthesizes findings from recent investigations and existing literature.
  • Analysis of evolutionary selective pressures on both APOBEC3 and Vif genes.

Main Results:

  • Lentiviral Vif evolved to antagonize mammalian APOBEC3 proteins.
  • Mammalian APOBEC3 genes are under selective pressure to escape Vif antagonism.
  • The interaction between APOBEC3 and Vif exemplifies an "evolutionary arms race."

Conclusions:

  • The APOBEC3-Vif interaction is a critical host-virus interface driving co-evolution.
  • Understanding this arms race provides insights into host-pathogen dynamics and viral adaptation.
Keywords:
APOBEC3Evolutionary arms raceLentivirusMammalVif

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