{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T13:05:04Z","timestamp":1792155904835,"version":"4.4.0"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2018,5,1]],"date-time":"2018-05-01T00:00:00Z","timestamp":1525132800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"Jilin University Science and Technology Innovative Research Team","award":["LUSTIRT 2017TD-05"],"award-info":[{"award-number":["LUSTIRT 2017TD-05"]}]},{"DOI":"10.13039\/501100002855","name":"Chinese Ministry of Science and Technology","doi-asserted-by":"crossref","award":["2012CB911102"],"award-info":[{"award-number":["2012CB911102"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002855","name":"Chinese Ministry of Science and Technology","doi-asserted-by":"crossref","award":["2013ZX10001-005"],"award-info":[{"award-number":["2013ZX10001-005"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Science and Technology Department of Jilin Province","award":["20160101044JC"],"award-info":[{"award-number":["20160101044JC"]}]},{"name":"Health and Family Planning Commission of Jilin Province","award":["2013Z066"],"award-info":[{"award-number":["2013Z066"]}]},{"name":"Key Laboratory of Molecular Virology, Jilin Province","award":["20102209"],"award-info":[{"award-number":["20102209"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81672004"],"award-info":[{"award-number":["81672004"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31270202"],"award-info":[{"award-number":["31270202"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The HIV-1 reservoir is a major obstacle to complete eradication of the virus. Although many proteins and RNAs have been characterized as regulators in HIV-1\/AIDS pathogenesis and latency, only a few long noncoding RNAs (lncRNAs) have been shown to be closely associated with HIV-1 replication and latency. In this study, we demonstrated that lncRNA uc002yug.2 plays a key role in HIV-1 replication and latency. uc002yug.2 potentially enhances HIV-1 replication, long terminal repeat (LTR) activity, and the activation of latent HIV-1 in both cell lines and CD4\n            <jats:sup>+<\/jats:sup>\n            T cells from patients. Further investigation revealed that uc002yug.2 activates latent HIV-1 through downregulating RUNX1b and -1c and upregulating Tat protein expression. The accumulated evidence supports our model that the Tat protein has the key role in the uc002yug.2-mediated regulatory effect on HIV-1 reactivation. Moreover, uc002yug.2 showed an ability to activate HIV-1 similar to that of suberoylanilide hydroxamic acid or phorbol 12-myristate 13-acetate using latently infected cell models. These findings improve our understanding of lncRNA regulation of HIV-1 replication and latency, providing new insights into potential targeted therapeutic interventions.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            The latent viral reservoir is the primary obstacle to curing HIV-1 disease. To date, only a few lncRNAs, which play major roles in various biological processes, including viral infection, have been identified as regulators in HIV-1 latency. In this study, we demonstrated that lncRNA uc002yug.2 is important for both HIV-1 replication and activation of latent viruses. Moreover, uc002yug.2 was shown to activate latent HIV-1 through regulating alternative splicing of RUNX1 and increasing the expression of Tat protein. These findings highlight the potential merit of targeting lncRNA uc002yug.2 as an activating agent for latent HIV-1.\n          <\/jats:p>","DOI":"10.1128\/jvi.01844-17","type":"journal-article","created":{"date-parts":[[2018,2,27]],"date-time":"2018-02-27T11:07:45Z","timestamp":1519729665000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":60,"title":["Long Noncoding RNA uc002yug.2 Activates HIV-1 Latency through Regulation of mRNA Levels of Various RUNX1 Isoforms and Increased Tat Expression"],"prefix":"10.1128","volume":"92","author":[{"given":"Chen","family":"Huan","sequence":"first","affiliation":[{"name":"The First Hospital of Jilin University, Institute of Virology and AIDS Research, Changchun, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhaolong","family":"Li","sequence":"additional","affiliation":[{"name":"The First Hospital of Jilin University, Institute of 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