Virology. 2009 Jun 20;389(1-2):20-5. Epub 2009 May 17.

TLR5 stimulation is sufficient to trigger reactivation of latent HIV-1 provirus in T lymphoid cells and activate virus gene expression in central memory CD4+ T cells.

Thibault S, Imbeault M, Tardif MR, Tremblay MJ.

Source

Centre de Recherche en Infectiologie, Centre Hospitalier de l'Université Laval; Faculté de Médecine, Université Laval, Québec G1V4G2, Canada.

Abstract

When effector CD4+ T cells carrying integrated HIV-1 proviruses revert back to a resting memory state, the virus can remain silent in those cells for years. Following re-exposure to the nominal antigen or in response to other stimuli (e.g. pro-inflammatory cytokines), these cells can begin to produce virus. Here we demonstrate that TLR5 stimulation induces activation of NF-kappaB and reactivate latent HIV-1 in CD4+ T lymphoid cells. Interestingly, we report also that TLR5 engagement leads to virus gene expression in quiescent central memory CD4+ T cells, a cell population recognized as a major reservoir in infected individuals. This study supports the hypothesis that translocation of microbes that can engage pathogen recognition receptors might play a dominant role in chronic immune activation seen in HIV-1-infected individuals and promote virus replication and dissemination.

PMID:: 19447460; [PubMed - indexed for MEDLINE]

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TLR5 stimulation is sufficient to trigger reactivation of latent HIV-1 provirus in T lymphoid cells and activate virus gene expression in central memory CD4+ T cells.

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