Reuschl, Ann-Kathrin; Mesner, Dejan; Shivkumar, Maitreyi; Whelan, Matthew VX; Pallett, Laura J; Guerra-Assunção, José Afonso; Madansein, Rajhmun; ... Jolly, Clare; + view all Reuschl, Ann-Kathrin; Mesner, Dejan; Shivkumar, Maitreyi; Whelan, Matthew VX; Pallett, Laura J; Guerra-Assunção, José Afonso; Madansein, Rajhmun; Dullabh, Kaylesh J; Sigal, Alex; Thornhill, John P; Herrera, Carolina; Fidler, Sarah; Noursadeghi, Mahdad; Maini, Mala K; Jolly, Clare; - view fewer (2022) HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells. Cell Reports , 39 (2) , Article 110650. 10.1016/j.celrep.2022.110650.

Preview

Text Pallett_PIIS2211124722004028.pdf - Published Version Download (50MB) | Preview

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 vitro to 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 TRM transcriptional 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.

Download activity - last month

Export as CSVXMLJSON

Download activity - last 12 months

Export as JSONXMLCSV

Downloads by country - last 12 months

Export as JSONXMLCSV

Archive Staff Only

View Item