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Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif

Roberto Mariani1, Darlene Chen, Bärbel Schröfelbauer

  • 1Infectious Disease Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.

Cell
|July 16, 2003
PubMed

Insights

The HIV-1 Vif protein prevents APOBEC3G from being packaged into new viruses, stopping viral replication. This interaction is species-specific, potentially limiting HIV-1 to human hosts.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • The HIV-1 accessory protein Vif (virion infectivity factor) is crucial for producing infectious virions.
  • Vif counters the antiviral activity of APOBEC3G, a cellular protein that inhibits viral replication by deaminating viral DNA.

Purpose of the Study:

  • To investigate the interaction between HIV-1 Vif and human and non-human primate APOBEC3G.
  • To understand the species-specificity of Vif-APOBEC3G interaction and its implications for HIV-1 restriction.

Main Methods:

  • Complex formation assays between HIV-1 Vif and human/mouse/AGM APOBEC3G.
  • Analysis of APOBEC3G encapsidation into HIV-1 virions in the presence of Vif.

Main Results:

  • HIV-1 Vif forms a complex with human APOBEC3G, preventing its encapsidation into virions.
  • HIV-1 Vif does not efficiently complex with mouse or AGM APOBEC3G, allowing their encapsidation.
  • Human APOBEC3G potently inhibits wild-type HIV-1 replication, unlike mouse or AGM APOBEC3G.

Conclusions:

  • The species-specific interaction between HIV-1 Vif and APOBEC3G restricts HIV-1 infection to humans.
  • Therapeutic strategies targeting the Vif-APOBEC3G interaction or boosting APOBEC3G could be beneficial for HIV-1 treatment.

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