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Despite the availability of antivirals against influenza, new IAV strains continue to persist by overcoming the therapeutics. Therefore, much emphasis in the field is placed on identifying new therapeutic targets that can more effectively control influenza. IAV utilizes several tactics to evade host innate immunity, which include the evasion of antiviral type I interferon (IFN) responses. Degradation of type I IFN receptor (IFNAR) is one known method of subversion, but the molecular mechanism for IFNAR downregulation during IAV infection remains unclear. Here, we have found that a host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR degradation and accelerates IAV replication. The findings reveal a novel cellular target for the potential development of antivirals against influenza, as well as expand our base of knowledge regarding interactions between influenza and the host innate immunity.<\/jats:p>","DOI":"10.1128\/jvi.01572-19","type":"journal-article","created":{"date-parts":[[2020,1,7]],"date-time":"2020-01-07T08:07:44Z","timestamp":1578384464000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":48,"title":["PARP1 Enhances Influenza A Virus Propagation by Facilitating Degradation of Host Type I Interferon Receptor"],"prefix":"10.1128","volume":"94","author":[{"given":"Chuan","family":"Xia","sequence":"first","affiliation":[{"name":"Department of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China"},{"name":"Departments of Surgery and Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri, 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