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
Virologyjournal_title
Virologyauthors
Thibault S,Imbeault M,Tardif MR,Tremblay MJdoi
10.1016/j.virol.2009.04.019subject
Has Abstractpub_date
2009-06-20 00:00:00pages
20-5issue
1-2eissn
0042-6822issn
1096-0341pii
S0042-6822(09)00279-7journal_volume
389pub_type
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