APOBEC3G-Depleted Resting CD4+ T Cells Remain Refractory to HIV1 Infection
Author(s) -
Francesca R. Santoni de Sio,
Didier Trono
Publication year - 2009
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0006571
Subject(s) - apobec3g , phenotype , reverse transcriptase , immunology , biology , human immunodeficiency virus (hiv) , microbiology and biotechnology , rna , virology , antibody , genetics , cytidine deaminase , gene
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom