{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:53:57Z","timestamp":1790776437635,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T00:00:00Z","timestamp":1756944000000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Tyrosine kinase non\u2010receptor2 (TNK2) is a host protein involved in vesicular trafficking, cell spreading, migration, survival, and proliferation. TNK2 has been identified as a conserved host factor for the entry of several non\u2010enveloped RNA viruses, such as Orsay virus in\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    and multiple picornaviruses in cells and mice. Although TNK2 was reported as required for influenza A virus infection in a genome\u2010wide CRISPR screen, its role remains contentious as it was not identified in other screens. In this study, we comprehensively evaluated TNK2's function in IAV infection using in vitro and in vivo models. RNAi knockdown and CRISPR knockout of\n                    <jats:italic>TNK2<\/jats:italic>\n                    in multiple cells showed no significant reduction in IAV infection. Similarly, primary lung fibroblasts and bone marrow\u2013derived macrophages from\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2010\/\u2010<\/jats:italic>\n                    <\/jats:sup>\n                    mice exhibited comparable infection to those from\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/+<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Moreover,\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2010\/\u2010<\/jats:italic>\n                    <\/jats:sup>\n                    mice exhibited no differences in weight loss, survival, lung pathology, or viral load compared to those of\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/+<\/jats:italic>\n                    <\/jats:sup>\n                    mice after IAV infection. Furthermore, the expression of interferon\u2010\u03b2 and interferon\u2010stimulated genes were not significantly altered in\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2010\/\u2010<\/jats:italic>\n                    <\/jats:sup>\n                    mice compared to that of\n                    <jats:italic>Tnk2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>+\/+<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Together, these results indicate that TNK2 is not a dominant host factor for IAV infection, suggesting it may not be a viable therapeutic target.\n                  <\/jats:p>","DOI":"10.1002\/jmv.70592","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T08:37:36Z","timestamp":1756975056000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Ablations of Human and Murine TNK2\/ACK1 Proteins Do Not Alter Influenza A Virus Infections In Vitro or In Vivo"],"prefix":"10.1002","volume":"97","author":[{"given":"Sisi","family":"Liu","sequence":"first","affiliation":[{"name":"School of Public Health (Shenzhen) Sun Yat\u2010sen University Shenzhen Guangdong China"},{"name":"Shenzhen Key Laboratory of Pathogenic Microbes and Biosafety Shenzhen Guangdong 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