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Corrigendum to "Sangivamycin is preferentially incorporated into viral RNA by the SARS-CoV-2 polymerase" [Antivir. Res. 218 (2023) 105716-105728, doi: 10.1016/j.antiviral.2023.105716].

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APOBEC3G: a double agent in defense.

Harold C Smith1

  • 1Department of Biochemistry and Biophysics, University of Rochester, School of Medicine and Dentistry, Rochester, NY 14642, USA. harold.smith@rochester.edu

Trends in Biochemical Sciences
|January 18, 2011
PubMed
Summary
This summary is machine-generated.

APOBEC3G (A3G) is a cellular defense protein against HIV. However, HIV

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • APOBEC3G (A3G) functions as a cellular host defense factor against HIV, particularly when the HIV-encoded protein Vif is absent.
  • Wild-type Vif targets A3G for proteasomal degradation, significantly reducing its antiviral capabilities.
  • Emerging evidence questions A3G's antiviral potency and suggests it may promote more virulent HIV strains.

Purpose of the Study:

  • To propose a new perspective on APOBEC3G's role in HIV infection.
  • To highlight A3G's potential dual function as both a defense factor and a promoter of viral virulence.
  • To advocate for further research into the regulatory mechanisms governing A3G's antiviral activity.

Main Methods:

  • This article is a conceptual review and synthesis of existing research.
  • It does not present new experimental data but analyzes current findings on A3G and Vif interactions.
  • Focuses on re-interpreting the known roles of A3G in the context of HIV evolution.

Main Results:

  • APOBEC3G (A3G) exhibits a dual role in HIV infection, acting as both a host defense mechanism and potentially promoting viral evolution.
  • The efficacy of A3G is critically dependent on the presence or absence of the HIV Vif protein.
  • Under certain conditions, A3G may inadvertently contribute to the emergence of more virulent HIV strains.

Conclusions:

  • APOBEC3G (A3G) should be recognized as a potential 'double agent' in the context of HIV.
  • Future research must elucidate the cellular and viral factors that modulate A3G's antiviral functions.
  • Development of novel research tools is crucial for understanding and potentially harnessing A3G's complex role.