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Two mechanisms have been raised for the preferential retention of HIV within Tfh CD4\n            <jats:sup>+<\/jats:sup>\n            T cells: (i) antiretroviral drugs have limited tissue distribution, resulting in insufficient tissue concentration and lower efficacy in controlling HIV replication in lymphoid tissues, and (ii) cytotoxic CD8\n            <jats:sup>+<\/jats:sup>\n            T cells within lymphoid tissues express low levels of chemokine receptor (CXCR5), thus limiting their ability to enter the GCs to control\/eliminate HIV-infected Tfh cells. Our results indicate that the BCL6 inhibitor FX1 can not only repress HIV infection of tonsillar Tfh\n            <jats:italic>ex vivo<\/jats:italic>\n            but also suppress HIV infection and reactivation in primary, non-Tfh CD4\n            <jats:sup>+<\/jats:sup>\n            T cells. Our study provides a rationale for targeting BCL6 protein to extend ART-mediated reduction of persistent HIV and\/or support strategies toward HIV remission beyond ART cessation.\n          <\/jats:p>","DOI":"10.1128\/jvi.01073-18","type":"journal-article","created":{"date-parts":[[2018,10,24]],"date-time":"2018-10-24T10:27:35Z","timestamp":1540376855000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":13,"title":["BCL6 Inhibitor-Mediated Downregulation of Phosphorylated SAMHD1 and T Cell Activation Are Associated with Decreased HIV Infection and Reactivation"],"prefix":"10.1128","volume":"93","author":[{"given":"Yanhui","family":"Cai","sequence":"first","affiliation":[{"name":"HIV-1 Immunopathogenesis Laboratory, The Wistar Institute, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Abdel-Mohsen","sequence":"additional","affiliation":[{"name":"HIV-1 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