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In this study, we identified a number of m\n                      <jats:sup>6<\/jats:sup>\n                      A modification sites within human T-cell leukemia virus type 1 (HTLV-1) RNAs, particularly in the RNA of the Tax oncogene. We demonstrated that YTH domain family member 2 (YTHDF2), a key m\n                      <jats:sup>6<\/jats:sup>\n                      A reader protein that binds m\n                      <jats:sup>6<\/jats:sup>\n                      A-modified RNAs and influences RNA metabolism, is required for HTLV-1 replication in both\n                      <jats:italic toggle=\"yes\">de novo<\/jats:italic>\n                      and persistently infected cells. Mechanistically, YTHDF2 interacts with and stabilizes Tax RNA in an m\n                      <jats:sup>6<\/jats:sup>\n                      A-dependent manner, thereby promoting Tax-driven HTLV-1 replication. Importantly, YTHDF2 activates oncogenic cellular pathways and promotes proliferation in HTLV-1-infected cells, aligning with the functions of Tax. Overall, our findings characterize YTHDF2 as a host factor critical to HTLV-1 RNA metabolism and viral propagation, offering novel insights into the understanding of the HTLV-1 life cycle and the development of targeted interventions.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        m\n                        <jats:sup>6<\/jats:sup>\n                        A is an RNA modification that plays crucial roles in physiological and pathological conditions; however, its roles in HTLV-1 infection are poorly understood. In this study, we identified that m\n                        <jats:sup>6<\/jats:sup>\n                        A modification is widely present in HTLV-1 RNAs, including Tax. We demonstrate that YTHDF2, a prominent m\n                        <jats:sup>6<\/jats:sup>\n                        A reader protein, enhances the stability of Tax RNA, thereby promoting both\n                        <jats:italic toggle=\"yes\">de novo<\/jats:italic>\n                        and persistent HTLV-1 replication. Our findings position YTHDF2 as an essential factor for HTLV-1 persistence and suggest it as a potential therapeutic target for viral clearance.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jvi.00529-26","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T13:00:01Z","timestamp":1778850001000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["The m\n                    <sup>6<\/sup>\n                    A reader protein YTHDF2 facilitates HTLV-1 infectious and mitotic propagation by stabilizing Tax RNA"],"prefix":"10.1128","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-5018-8432","authenticated-orcid":false,"given":"Yi","family":"Liang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01sfm2718","id-type":"ROR","asserted-by":"publisher"}],"name":"State Key Laboratory 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