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- W4289766520 abstract "SUMMARY Deciphering the mechanisms underlying viral persistence is critical to achieving a cure for HIV infection. We implemented a systems approach to discover molecular signatures of HIV latently-infected CD4+ T cells, identifying the immunosuppressive, adenosine-producing ectonucleotidase CD73 as a key surface marker of latent cells. Hypoxic conditioning, reflecting the lymphoid tissue microenvironment, increased the frequency of CD73+ CD4+ T cells and promoted HIV latency. Transcriptomic profiles of CD73+ CD4+ T cells favored viral quiescence, immune evasion, and cell survival. CD73+ CD4+ T cells were capable of harboring a functional HIV reservoir and reinitiating productive infection ex vivo . CD73 or adenosine receptor blockade facilitated latent HIV reactivation in vitro , mechanistically linking adenosine signaling to viral quiescence. Finally, tissue imaging of lymph nodes from HIV-infected individuals on antiretroviral therapy revealed spatial association between CD73 expression and HIV persistence in vivo . Our findings warrant development of HIV cure strategies targeting the hypoxia-CD73-adenosine axis." @default.
- W4289766520 created "2022-08-04" @default.
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- W4289766520 date "2022-08-04" @default.
- W4289766520 modified "2023-09-27" @default.
- W4289766520 title "The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency" @default.
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- W4289766520 doi "https://doi.org/10.1101/2022.08.03.502655" @default.
- W4289766520 hasPublicationYear "2022" @default.
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