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.

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.

journal_name

Virology

journal_title

Virology

authors

Thibault S,Imbeault M,Tardif MR,Tremblay MJ

doi

10.1016/j.virol.2009.04.019

subject

Has Abstract

pub_date

2009-06-20 00:00:00

pages

20-5

issue

1-2

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(09)00279-7

journal_volume

389

pub_type

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