{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T01:09:49Z","timestamp":1789434589316,"version":"build-2803163510"},"reference-count":40,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T00:00:00Z","timestamp":1657152000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Given the frequent emergence of drug-resistant influenza virus strains and new highly pathogenic influenza virus strains, there is an urgent need to identify new antiviral drugs and targets. We found that influenza A virus (IAV) infection caused a significant decrease of microRNA let-7 expression in host cells; that overexpression of let-7 increased interferon expression and effectively inhibit IAV infection; and that let-7 targets the 3\u2019-untranslated region (UTR) of the ribosomal protein 16 (\n                    <jats:italic>RPS16<\/jats:italic>\n                    ) gene, decreasing its expression. Knocking down the expression of\n                    <jats:italic>RPS16<\/jats:italic>\n                    increased the expression of type I interferon and inhibited viral replication. The present study uncovered the regulatory effect of let-7b and let-7f on influenza A infection, which is a potential biomarker of IAV infection. In addition, let-7 may be a promising therapeutic agent against influenza A.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2022.904775","type":"journal-article","created":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T05:19:49Z","timestamp":1657171189000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":19,"title":["MicroRNA let-7 Suppresses Influenza A Virus Infection by Targeting RPS16 and Enhancing Type I Interferon Response"],"prefix":"10.3389","volume":"12","author":[{"given":"Wenjiao","family":"Wu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changliang","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuwen","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinghua","family":"Mei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,7,7]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"823","DOI":"10.1016\/S0092-8674(01)00616-X","article-title":"microRNAs: Tiny Regulators With Great Potential","volume":"107","author":"Ambros","year":"2001","journal-title":"Cell"},{"key":"B2","doi-asserted-by":"publisher","first-page":"350","DOI":"10.1038\/nature02871","article-title":"The Functions of Animal microRNAs","volume":"431","author":"Ambros","year":"2004","journal-title":"Nature"},{"key":"B3","doi-asserted-by":"publisher","first-page":"113","DOI":"10.1016\/j.virol.2015.05.017","article-title":"Dengue Virus NS1 Protein Interacts With the Ribosomal Protein RPL18: This Interaction is Required for Viral Translation and Replication in Huh-7 Cells","volume":"484","author":"ervantes-Salazar","year":"2015","journal-title":"Virology"},{"key":"B4","doi-asserted-by":"publisher","first-page":"1495","DOI":"10.1007\/s00705-017-3226-3","article-title":"miR-146a Negatively Regulates the Induction of Proinflammatory Cytokines in Response to Japanese Encephalitis Virus Infection in Microglial Cells","volume":"162","author":"Deng","year":"2017","journal-title":"Arch. 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