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APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction

Sharee Leong1,2, Hesham Nasser1, Terumasa Ikeda1

  • 1Division of Molecular Virology and Genetics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto 860-0811, Japan.

International Journal of Molecular Sciences
|February 26, 2025
PubMed

Insights

The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3/A3) family acts as an innate immune defense against retroviruses. This review explores how A3 editing and non-editing functions impact viral infections like HIV-1 and HTLV-1.

Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3/A3) family are crucial innate immune factors.
  • APOBEC3 proteins restrict retroviral and retroelement replication through DNA editing and other mechanisms.
  • Understanding A3-mediated restriction is vital for controlling retroviral infections.

Purpose of the Study:

  • To review the mechanisms of APOBEC3 (A3) restriction against retroviruses.
  • To examine the roles of A3 editing and non-editing activities in viral infection outcomes.
  • To focus on interactions between A3 proteins and human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus type 1 (HTLV-1).

Main Methods:

  • Literature review of studies on APOBEC3 proteins and retroviruses.
  • Analysis of research on A3 editing (cytosine-to-uracil conversion) and non-editing antiviral mechanisms.
  • Comparative examination of A3 interactions with HIV-1 and HTLV-1.

Main Results:

  • APOBEC3 proteins exhibit potent antiviral activity through both direct DNA editing and deaminase-independent pathways.
  • Editing activity leads to lethal mutations in viral genomes, while non-editing mechanisms can block viral replication steps.
  • Viral factors modulate the effectiveness of A3 restriction, influencing infection dynamics.

Conclusions:

  • APOBEC3 proteins are critical determinants of retroviral infection outcomes.
  • Both editing and non-editing functions of A3s contribute significantly to innate immunity against viruses like HIV-1 and HTLV-1.
  • Further research into A3-retrovirus interactions can inform therapeutic strategies against viral diseases.
Keywords:
APOBEC3 family proteinsHIV-1HTLV-1deaminase-dependent mechanismsdeaminase-independent mechanismsretrovirus restriction

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