https://socictopen.socict.org/files/original/f68cfa3d886d2fd6402fd2cd2e0cf4e3.pdf 904e7cd41ebb063e00208738043f8a0d Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Coronavirus Description An account of the resource Dominio científico: Coronavirus Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis Creator An entity primarily responsible for making the resource Lu Wang, Li Feng, Keliang Wang, Mei Xue, Fang Fu, Wanhai Xu, Changlin Wang, Ziqi Wang, Pinghuang Liu, Ling-Ling Shan, Shuxin Qu Description An account of the resource Porcine epidemic diarrhea virus (PEDV) is an economically important pathogen that has evolved several mechanisms to evade type I IFN responses. Type III interferon (IFN-λ), an innate cytokine that primarily targets the mucosal epithelia, is critical in fighting mucosal infection in the host and has been reported to potently inhibit PEDV infection in vitro. However, how PEDV escapes IFN-λ antiviral response remains unclear. In this study, we found that PEDV infection induced significant IFN-λ expression in type I IFN-defective Vero E6 cells, but virus-induced endogenous IFN-λ did not reduce PEDV titers. Moreover, we demonstrated that PEDV escaped IFN-λ responses by substantially upregulating the suppressor of cytokine signaling protein 1 (SOCS1) expression, which impaired the induction of IFN-stimulated genes (ISGs) and dampened the IFN-λ antiviral response and facilitated PEDV replication in Vero E6 cells. We further showed that PEDV infection increased SOCS1 expression by decreasing host miR-30c-5p expression. MiR-30c-5p suppressed SOCS1 expression through targeting the 3′ untranslated region (UTR) of SOCS1. The inhibition of IFN-λ elicited ISGs expression by SOCS1 was specifically rescued by overexpression of miR-30c-5p. Collectively, our findings identify a new strategy by PEDV to escape IFN-λ-mediated antiviral immune responses by engaging the SOCS1/miR-30c axis, thus improving our understanding of its pathogenesis. Date A point or period of time associated with an event in the lifecycle of the resource 2020 Subject The topic of the resource microRNA, coronavirus, PEDV, SOCS-1, IFN-λ, miR-30c-5p Identifier An unambiguous reference to the resource within a given context DOI: 10.3389/fmicb.2020.01180 Source A related resource from which the described resource is derived Frontiers in Microbiology Publisher An entity responsible for making the resource available Frontiers Media S.A. Coverage The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant Microbiology