HIV-1 Vpr Drives a B Cell-Like Phenotype in Primary CD4⁺ T Cells.

Authors

Peipei Wang, Jieying Li, Wei Wang, Zhuoyue Meng, Huixin Wu, Shumin Du, Kai Deng, Jinfeng Cai

Published in

MedComm. Volume 7. Issue 10. Pages e71018. Epub Sep 27, 2026.

Abstract

CD4⁺ T cells are the principal cellular targets of HIV-1, yet the extent to which viral proteins reshape their transcriptional identity remains incompletely understood. Here, using an integrated multi-omics approach, we identified a distinct population of HIV-1 RNA-positive CD4⁺ T cells that localized within transcriptionally defined B-cell clusters and expressed multiple canonical B cell-associated genes during acute infection. Mechanistic analyses revealed that this phenotype was driven by the HIV-1 accessory protein Vpr. Both Vpr overexpression and Vpr-deficient viral systems demonstrated that Vpr induces the expression of CD19, MS4A1, CD22, and PAX5 in primary CD4⁺ T cells. Single-cell RNA sequencing, bulk RNA sequencing, and assay for transposase-accessible chromatin using sequencing (ATAC-seq) further showed that Vpr promotes extensive transcriptional and epigenetic remodeling, accompanied by increased accessibility and expression of genes involved in B-cell differentiation and development, including PAX5, EBF1, and PRDM1. Notably, this B cell-like transcriptional program was transient and gradually diminished during prolonged culture. Together, our findings uncover an unexpected role of Vpr in inducing lineage-associated transcriptional reprogramming in mature CD4⁺ T cells and provide new insight into how HIV-1 manipulates host-cell identity during infection.

PMID:
42802798
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.

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