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APOBEC-1 cofactors regulate APOBEC3-induced mutations in hepatitis B virus.

Zhigang Chen1, Thomas L Eggerman1,2, Alexander V Bocharov1

  • 1Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA.

Journal of Virology
|January 27, 2025
PubMed
Summary
This summary is machine-generated.

APOBEC3 proteins (A3s) are crucial for immunity and cancer. This study reveals that APOBEC-1 (A1) cofactors and hnRNPs regulate A3 mutational activity, impacting viral defense and cancer mutations.

Keywords:
APOBEC3cofactorhepatitis B virushnRNPhypermutationmutationregulation

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Area of Science:

  • * Molecular biology
  • * Virology
  • * Cancer genetics

Background:

  • * APOBEC3 (A3) proteins are key host factors in innate immunity against viruses and in driving cancer mutations.
  • * The regulatory mechanisms governing A3 protein activity and the variability in A3-induced mutations remain largely unexplored.
  • * A3s function in complexes, and their family member APOBEC-1 (A1) requires cofactors for activity, suggesting a similar regulatory pathway for A3s.

Purpose of the Study:

  • * To investigate the role of A1 cofactors and associated heterogeneous nuclear ribonucleoproteins (hnRNPs) in regulating A3 mutational activity.
  • * To elucidate how these factors influence A3s' interaction with DNA substrates and their mutational efficiency.
  • * To understand the differential impact of A3 regulation on viral genomes versus human cancer mutations.

Main Methods:

  • * Utilized hepatitis B virus (HBV) cellular replication as a model system to study A3 activity.
  • * Employed co-expression and gene knockdown (siRNA) strategies to assess the impact of A1 cofactors and hnRNPs.
  • * Performed mutagenesis on A3G and A3B to disrupt protein interactions with hnRNPs.
  • * Conducted HBV genome-wide mutation analyses to evaluate A3C accessibility and mutational efficiency.

Main Results:

  • * A1 cofactors and hnRNPs were found to be involved in regulating A3 mutational activity, with effects varying based on A3 association strength (A3C > A3G > A3B).
  • * Co-expression of A1 cofactors significantly increased A3 mutational activity, while knockdown decreased it.
  • * Disruption of A3-hnRNP interactions via mutagenesis substantially reduced A3 mutational activity.
  • * A1 cofactors enhanced A3C accessibility to HBV DNA and promoted kataegis-like hypermutations.

Conclusions:

  • * A1 cofactors and hnRNPs are essential regulators of A3 mutational activity, interacting closely with A3 proteins.
  • * These cellular factors play a significant role in modulating A3-induced mutations under physiological conditions.
  • * Understanding A3-associated factor interactions offers potential therapeutic targets for controlling A3-driven mutations in cancer.