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

@article{citeulike:5452681, 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.}, author = {Santoni de Sio, Francesca R. and Trono, Didier}, citeulike-article-id = {5452681}, citeulike-linkout-0 = {http://dx.doi.org/10.1371/journal.pone.0006571}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19668336}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19668336}, doi = {10.1371/journal.pone.0006571}, issn = {1932-6203}, journal = {PloS one}, keywords = {apobec, infection}, number = {8}, posted-at = {2009-08-17 16:21:17}, priority = {2}, title = {APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection.}, url = {http://dx.doi.org/10.1371/journal.pone.0006571}, volume = {4}, year = {2009} }

TY - JOUR ID - citeulike:5452681 L3 - citeulike-article-id:5452681 N2 - 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. IS - 8 JF - PloS one SN - 1932-6203 TI - APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection. VL - 4 KW - apobec KW - infection AU - Santoni de Sio, Francesca AU - Trono, Didier PY - 2009/// UR - http://dx.doi.org/10.1371/journal.pone.0006571 ER -