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The incorporation of APOBEC3 proteins into murine leukemia viruses

Li Zhang1, Xiaoyu Li, Jing Ma

  • 1Department of Virology, Institute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing 100050, China.

Virology
|June 24, 2008
PubMed

Insights

Murine APOBEC3 (mA3) is less incorporated into Moloney murine leukemia virus (MLV) than human APOBEC3G (hA3G) due to MLV’s nucleocapsid domain. This inefficient incorporation allows MLV to evade mA3 antiviral activity.

Area of Science:

  • Retroviral replication
  • Innate immunity
  • Antiviral mechanisms

Background:

  • APOBEC3 proteins are crucial intrinsic antiviral factors that restrict retroviral replication.
  • Murine APOBEC3 (mA3) inhibits HIV-1 but not Moloney murine leukemia virus (MLV).
  • The differential activity suggests variations in APOBEC3 incorporation into different retroviruses.

Purpose of the Study:

  • To investigate the mechanisms underlying the differential incorporation of mA3 into HIV-1 and MLV.
  • To identify viral factors responsible for mA3 exclusion from MLV particles.
  • To elucidate the role of APOBEC3 protein domains and viral protein interactions in viral packaging.

Main Methods:

  • Comparative analysis of mA3 and hA3G incorporation into HIV-1 and MLV virions.
  • Site-directed mutagenesis and domain swapping studies involving the nucleocapsid (NC) domains of HIV-1 and MLV.
  • Investigation of interactions between mA3 and viral Gag proteins.

Main Results:

  • mA3 is incorporated less efficiently into MLV compared to HIV-1, while mA3 and hA3G incorporation into HIV-1 is similar.
  • The MLV nucleocapsid (NC) domain, unlike the HIV-1 NC domain, fails to facilitate mA3/Gag interaction, leading to mA3 exclusion from MLV.
  • The linker region between zinc coordination motifs in mA3 mediates interaction with HIV-1 Gag, similar to hA3G.

Conclusions:

  • The interaction between viral NC domains and APOBEC3 linker regions is a key mechanism for viral incorporation of these antiviral proteins.
  • MLV's inability to facilitate mA3/Gag interaction via its NC domain is responsible for excluding mA3.
  • Inefficient mA3 incorporation is a viral strategy for MLV to escape the inhibitory effects of endogenous mA3.

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