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APOBEC3-mediated editing in HIV type 1 from pediatric patients and its association with APOBEC3G/CUL5 polymorphisms

Federico A De Maio1, Carlos A Rocco, Paula C Aulicino

  • 1Laboratorio de Biología Celular y Retrovirus-CONICET, Hospital de Pediatría Prof. Dr. Juan P. Garrahan, Ciudad de Buenos Aires, Argentina.

AIDS Research and Human Retroviruses
|December 8, 2011
PubMed

Insights

APOBEC3-mediated editing of HIV-1 DNA, which can impact viral mutation and diversification, was analyzed in children. Host and viral genetic factors, not APOBEC3 activity, influenced editing levels and HIV-1 progression.

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • APOBEC3 proteins are cytidine deaminases that induce G→A mutations in HIV-1 DNA.
  • HIV-1 Vif protein counteracts APOBEC3 by targeting them for proteasomal degradation via a CUL5-based ubiquitin ligase complex.
  • APOBEC3 editing can inhibit HIV-1 replication through hypermutation or drive viral diversification and escape variants.

Purpose of the Study:

  • To analyze APOBEC3-mediated editing in perinatally HIV-1 infected children.
  • To explore associations between APOBEC3 editing, host genetic polymorphisms (APOBEC3G, CUL5), HIV-1 Vif variability, and time to AIDS development.
  • To develop a novel index for quantifying APOBEC3 editing levels in HIV-1 proviral DNA.

Main Methods:

  • Analysis of proviral HIV-1 DNA from 93 perinatally infected children.
  • Genotyping of APOBEC3G and CUL5 gene polymorphisms (APOBEC3G H186R, APOBEC3G C40693T, CUL5 SNP6).
  • Sequencing of HIV-1 Vif gene variants.
  • Development of a quantitative index for APOBEC3 editing using the HIV-1 pol gene's central polypurine tract (cPPT).

Main Results:

  • Reduced APOBEC3-mediated editing was associated with the CUL5 SNP6 minor allele.
  • Specific HIV-1 Vif variants (mutations at sites 46, 122, and 160) correlated with reduced editing.
  • No significant impact of APOBEC3 activity on disease progression (time to AIDS) was detected.

Conclusions:

  • APOBEC3-mediated editing of HIV-1 in pediatric infections is modulated by host (CUL5) and viral (Vif) genetic factors.
  • The findings suggest complex interactions influencing viral evolution and pathogenesis in children.
  • Further research is needed to fully elucidate the interplay between host genetics, viral factors, and APOBEC3 editing in HIV-1 infection.

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