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APOBEC3G: an intracellular centurion.

Ya-Lin Chiu1, Warner C Greene

  • 1Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|November 15, 2008
PubMed
Summary
This summary is machine-generated.

The APOBEC3G (A3G) protein restricts HIV-1 infection in two forms: low-molecular-mass (LMM) A3G fights external viruses, while high-molecular-mass (HMM) A3G combats internal retroelements.

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Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • APOBEC3G (A3G) is a key intrinsic antiretroviral factor active against HIV-1.
  • A3G exists in distinct low-molecular-mass (LMM) and high-molecular-mass (HMM) forms with differing biological activities.
  • Resting CD4 T cells harbor LMM A3G, which potently restricts HIV-1 post-entry.

Purpose of the Study:

  • To elucidate the distinct roles of LMM and HMM A3G in cellular defense.
  • To understand how T-cell activation influences A3G localization and function.
  • To investigate HIV-1's mechanism for evading A3G restriction in activated T cells.

Main Methods:

  • Analysis of A3G localization and complex formation in resting versus activated CD4 T cells.
  • Investigation of the role of Alu/hY retroelement RNAs in HMM A3G complex nucleation.
  • Assessment of A3G encapsidation into HIV-1 virions under varying conditions (Vif presence/absence).

Main Results:

  • Activated T cells recruit LMM A3G into HMM complexes, likely mediated by induced Alu/hY RNAs.
  • HMM A3G complexes sequester retroelement RNAs, preventing their retrotransposition.
  • HIV-1 exploits the depletion of LMM A3G in activated T cells for productive infection.
  • LMM A3G is preferentially packaged into HIV-1 virions when Vif is absent.

Conclusions:

  • LMM A3G acts as a primary defense against exogenous retroviruses like HIV-1.
  • HMM A3G complexes provide defense against endogenous retroelements, such as Alu/hY.
  • HIV-1 utilizes T-cell activation to overcome A3G-mediated restriction by depleting the active LMM form.