APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection

Francesca R. Santoni de Sio, Didier Trono

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Background: CD4+ T lymphocytes are the primary targets of HIV1 but cannot be infected when fully quiescent, due to a post-entry block preventing the completion of reverse transcription. Chiu et al. recently proposed that this restriction reflects the action of APOBEC3G (A3G). They further suggested that T cell activation abrogates the A3G-mediated block by directing this protein to a high molecular mass complex. Methodology/Principal Findings: In the present work, we sought to explore further this model. However, we found that effective suppression of A3G by combined RNA interference and expression of HIV1 Vif does not relieve the restrictive phenotype of post-activation resting T cells. We also failed to find a correlation between HIV resistance and the presence of A3G in a low molecular complex in primary T cells. Conclusions/Significance: We conclude that A3G is unlikely to play a role in the HIV restrictive phenotype of quiescent T lymphocytes.

Original languageEnglish
Article numbere6571
JournalPLoS One
Volume4
Issue number8
DOIs
Publication statusPublished - Aug 10 2009

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T-cells
Refractory materials
T-lymphocytes
T-Lymphocytes
Infection
infection
Chemical activation
HIV
Phenotype
phenotype
reverse transcription
Molecular mass
Transcription
RNA Interference
RNA interference
Reverse Transcription
RNA
molecular weight
Proteins
proteins

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection. / Santoni de Sio, Francesca R.; Trono, Didier.

In: PLoS One, Vol. 4, No. 8, e6571, 10.08.2009.

Research output: Contribution to journalArticle

Santoni de Sio, Francesca R. ; Trono, Didier. / APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection. In: PLoS One. 2009 ; Vol. 4, No. 8.
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