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


RESULTS
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
We conclude that A3G is unlikely to play a role in the HIV restrictive phenotype of quiescent T lymphocytes.
Santoni de Sio
Francesca R
FR
Global Health Institute, School of Life Sciences, Frontiers in Genetics National Center of Competence in Research, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Trono
Didier
D
D000071478:APOBEC Deaminases; D015153:Blotting, Western; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003564:Cytidine Deaminase; D043525:Cytosine Deaminase / Q000235:genetics / Q000276:immunology*; D005434:Flow Cytometry; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1; D006801:Humans; D014461:Ultracentrifugation
D043525:Cytosine Deaminase; D000071478:APOBEC Deaminases; C502889:APOBEC3 proteins, human; D003564:Cytidine Deaminase