{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T21:21:29Z","timestamp":1788297689073,"version":"build-2803163510"},"reference-count":62,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,7,23]],"date-time":"2013-07-23T00:00:00Z","timestamp":1374537600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008920","name":"University of Saskatchewan","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100008920","id-type":"DOI","asserted-by":"crossref"}]},{"name":"National Science and Engineering Research Foundation","award":["RGPIN-342475"],"award-info":[{"award-number":["RGPIN-342475"]}]},{"DOI":"10.13039\/501100000106","name":"Saskatchewan Health Research Foundation","doi-asserted-by":"crossref","award":["RAPID 1927"],"award-info":[{"award-number":["RAPID 1927"]}],"id":[{"id":"10.13039\/501100000106","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["WIREs RNA"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:p>The unusual role for <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 in promoting the hepatitis C virus (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>) life cycle was first identified in 2005, but its mechanism of action remains uncharacterized. The virus appears to use the microRNA (<jats:styled-content style=\"fixed-case\">miRNA<\/jats:styled-content>) in a way that is opposed to that of normal <jats:styled-content style=\"fixed-case\">miRNAs<\/jats:styled-content>. Instead of interacting with sequences in the 3\u2032\u2010untranslated region (<jats:styled-content style=\"fixed-case\">UTR<\/jats:styled-content>), <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 binds to two sites in the 5\u2032\u2010<jats:styled-content style=\"fixed-case\">UTR<\/jats:styled-content>, and instead of silencing gene expression or promoting the degradation of the viral <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>, it stabilizes the genome and potently augments the efficiency by which <jats:styled-content style=\"fixed-case\">HCV RNA<\/jats:styled-content> accumulates in infected cells. This review discusses the current knowledge and models for the mechanism by which <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 promotes the <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> life cycle. Annealing of <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 to the <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> genome requires particular base pairing, stimulates translation, and stabilizes the viral genome by blocking degradation by host exonucleases, but these functions are unlikely to be the whole story. We will discuss other possible functions for <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122, the stages of the <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> life cycle at which <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 may influence <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>, and other related viruses that may be similarly regulated by <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122. Despite our lack of detailed mechanistic information, antagonism of <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 is emerging as a powerful method to inhibit <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> infections, and unique to other <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> treatment strategies does not, thus far, appear to induce emergence of escape mutants. Used alone or in combination with other antiviral drugs, <jats:styled-content style=\"fixed-case\">miR<\/jats:styled-content>\u2010122 antagonists could be useful to both inhibit the virus and provide selective pressure to inhibit the development of resistance. <jats:italic>WIREs RNA<\/jats:italic> 2013, 4:665\u2013676. doi: 10.1002\/wrna.1186<\/jats:p><jats:p>This article is categorized under:\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>RNA Turnover and Surveillance &gt; Regulation of RNA Stability<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Regulatory RNAs\/RNAi\/Riboswitches &gt; RNAi: Mechanisms of Action<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Regulatory RNAs\/RNAi\/Riboswitches &gt; Regulatory RNAs<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>RNA in Disease and Development &gt; RNA in Disease<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p>","DOI":"10.1002\/wrna.1186","type":"journal-article","created":{"date-parts":[[2013,7,24]],"date-time":"2013-07-24T13:40:15Z","timestamp":1374673215000},"page":"665-676","source":"Crossref","is-referenced-by-count":25,"title":["<scp>miR<\/scp>\u2010122 Promotion of the hepatitis C virus life cycle: sound in the silence"],"prefix":"10.1002","volume":"4","author":[{"given":"Joyce A.","family":"Wilson","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology University of Saskatchewan Saskatoon Canada"},{"name":"VIDO\u2010Intervac University of Saskatchewan Saskatoon Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Huys","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology University of Saskatchewan Saskatoon Canada"},{"name":"VIDO\u2010Intervac University of Saskatchewan Saskatoon 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