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HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells
- Source :
- Cell Reports; April 2022, Vol. 39 Issue: 2
- Publication Year :
- 2022
-
Abstract
- HIV-1 replicates in CD4+T cells, leading to AIDS. Determining how HIV-1 shapes its niche to create a permissive environment is central to informing efforts to limit pathogenesis, disturb reservoirs, and achieve a cure. A key roadblock in understanding HIV-T cell interactions is the requirement to activate T cells in vitroto make them permissive to infection. This dramatically alters T cell biology and virus-host interactions. Here we show that HIV-1 cell-to-cell spread permits efficient, productive infection of resting memory T cells without prior activation. Strikingly, we find that HIV-1 infection primes resting T cells to gain characteristics of tissue-resident memory T cells (TRM), including upregulating key surface markers and the transcription factor Blimp-1 and inducing a transcriptional program overlapping the core TRMtranscriptional signature. This reprogramming is driven by Vpr and requires Vpr packaging into virions and manipulation of STAT5. Thus, HIV-1 reprograms resting T cells, with implications for viral replication and persistence.
Details
- Language :
- English
- ISSN :
- 22111247
- Volume :
- 39
- Issue :
- 2
- Database :
- Supplemental Index
- Journal :
- Cell Reports
- Publication Type :
- Periodical
- Accession number :
- ejs59418596
- Full Text :
- https://doi.org/10.1016/j.celrep.2022.110650