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Status of APOBEC3G/F in cells and progeny virions modulated by Vif determines HIV-1 infectivity

Tomoki Yamashita1, Masako Nomaguchi, Ariko Miyake

  • 1Department of Microbiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan.

Microbes and Infection
|December 1, 2009
PubMed

Insights

This study investigated how HIV-1 Vif protein interacts with APOBEC3G/3F proteins. Vif binding to A3G/A3F is essential for HIV-1 infectivity and viral particle formation.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Human Immunodeficiency Virus type 1 (HIV-1) utilizes the Vif protein to counteract host restriction factors.
  • APOBEC3G (A3G) and APOBEC3F (A3F) are host antiviral proteins that inhibit HIV-1 replication.
  • The interaction between Vif and A3G/A3F is crucial for viral pathogenesis.

Purpose of the Study:

  • To elucidate the specific roles of HIV-1 Vif mutants in interacting with APOBEC3G and APOBEC3F.
  • To determine the impact of Vif-APOBEC3 interactions on viral infectivity and virion composition.

Main Methods:

  • Construction and analysis of replication-defective HIV-1 Vif mutants.
  • Assessment of A3G/A3F incorporation into viral particles (virions).
  • Evaluation of Vif binding to A3G/A3F in cellular and virion contexts.

Main Results:

  • All replication-defective Vif mutants incorporated A3G/A3F into virions.
  • A specific mutant Vif bound A3G in cells but not in virions.
  • Another Vif mutant suppressed A3F activity without excluding it from virions.
  • Vif incorporation into virions was dependent on its interaction with A3G/A3F.

Conclusions:

  • Functional binding of Vif to A3G/A3F, either in cells or virions, is critical for HIV-1 infectivity.
  • Different Vif-APOBEC3 interaction mechanisms can influence viral replication and restriction factor evasion.

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