{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T05:45:13Z","timestamp":1792043113593,"version":"4.4.0"},"reference-count":79,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:00:00Z","timestamp":1790467200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:00:00Z","timestamp":1790467200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82302514"],"award-info":[{"award-number":["82302514"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MedComm"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells are the principal cellular targets of HIV\u20101, yet the extent to which viral proteins reshape their transcriptional identity remains incompletely understood. Here, using an integrated multi\u2010omics approach, we identified a distinct population of HIV\u20101 RNA\u2010positive CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells that localized within transcriptionally defined B\u2010cell clusters and expressed multiple canonical B cell\u2010associated genes during acute infection. Mechanistic analyses revealed that this phenotype was driven by the HIV\u20101 accessory protein Vpr. Both Vpr overexpression and Vpr\u2010deficient viral systems demonstrated that Vpr induces the expression of CD19, MS4A1, CD22, and PAX5 in primary CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Single\u2010cell RNA sequencing, bulk RNA sequencing, and assay for transposase\u2010accessible chromatin using sequencing (ATAC\u2010seq) further showed that Vpr promotes extensive transcriptional and epigenetic remodeling, accompanied by increased accessibility and expression of genes involved in B\u2010cell differentiation and development, including PAX5, EBF1, and PRDM1. Notably, this B cell\u2010like transcriptional program was transient and gradually diminished during prolonged culture. Together, our findings uncover an unexpected role of Vpr in inducing lineage\u2010associated transcriptional reprogramming in mature CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells and provide new insight into how HIV\u20101 manipulates host\u2010cell identity during infection.\n                  <\/jats:p>","DOI":"10.1002\/mco2.71018","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T13:32:14Z","timestamp":1790515934000},"source":"Crossref","is-referenced-by-count":0,"title":["HIV\u20101 Vpr Drives a B Cell\u2010Like Phenotype in Primary CD4\n                    <sup>+<\/sup>\n                    T Cells"],"prefix":"10.1002","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5397-5579","authenticated-orcid":false,"given":"Peipei","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases The Third Affiliated Hospital Sun Yat\u2010sen University  Guangzhou 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