Abstract：
:HIV persists in latently infected CD4+ T cells during antiretroviral therapy (ART). Immune checkpoint molecules, including PD-1, are preferentially expressed at the surface of persistently infected cells. However, whether PD-1 plays a functional role in HIV latency and reservoir persistence remains unknown. Using CD4+ T cells from HIV-infected individuals, we show that the engagement of PD-1 inhibits viral production at the transcriptional level and abrogates T-cell receptor (TCR)-induced HIV reactivation in latently infected cells. Conversely, PD-1 blockade with the monoclonal antibody pembrolizumab enhances HIV production in combination with the latency reversing agent bryostatin without increasing T cell activation. Our results suggest that the administration of immune checkpoint blockers to HIV-infected individuals on ART may facilitate latency disruption.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Fromentin R,DaFonseca S,Costiniuk CT,El-Far M,Procopio FA,Hecht FM,Hoh R,Deeks SG,Hazuda DJ,Lewin SR,Routy JP,Sékaly RP,Chomont Ndoi
10.1038/s41467-019-08798-7subject
Has Abstractpub_date
2019-02-18 00:00:00pages
814issue
1issn
2041-1723pii
10.1038/s41467-019-08798-7journal_volume
10pub_type
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