LAUSR

ABSTRACT The regulation of interferon‐&agr; signaling pathways is essential to protect the host from infection with a broad range of viruses. However, information regarding antiviral response and the specific molecular mechanism of Columba livia interferon‐&agr; (CoIFN‐&agr;) has not been reported to date. In this study, we cloned a 723bp complete ORF of CoIFN‐&agr; gene. The specific antiviral activity of CoIFN‐&agr; in VSV (TCID50 = 10−5.87/100 &mgr;L)‐infected CEFs reached 5.5 × 105 U/mg. Moreover, our result indicated that the anti‐VSV efficient of CoIFN‐&agr; might depend on the expression of NF‐&kgr;B. CoIFN‐&agr; also showed high sensitivity to trypsin and relatively stable after acid, alkali or heat treatment. Moreover, CoIFN‐&agr; activated STAT/Jak signaling and autophagy to inhibit VSV‐induced apoptosis. Although the expression of p53 was further increased, apoptosis was not involved in CoIFN‐&agr; against VSV. Notably, although STAT signaling was efficiently activated, knockdown p53 did inhibit the antiviral activity of the CoIFN‐&agr; via decreasing the expression of Mx1 but not weakened Jak phosphorylation. Moreover, VSV aggravated the apoptosis and the expression of cleaved Mdm2 in knockdown p53 under preincubated CoIFN‐&agr;. Taken together, p53 might as a highly interconnected regulator in IFN‐&agr; antiviral response and cleaved Mdm2 might as a dominant‐negative regulator by competing with full length Mdm2 for p53 binding in virus infection. Overall, our research not only enriches CoIFN‐&agr; antiviral features but also helps explain that p53 enhance the CoIFN‐&agr; antiviral response against pigeon viral diseases. HighlightsThe characterization and biological activity of Columba livia IFN‐&agr; were analyzed.Columba livia IFN‐&agr; project protective effects on virus‐induced apoptosis.NF‐&kgr;B is involved in the antiviral activity between CoIFN‐&agr; and ChIFN‐&agr; resisted VSV.Knockdown p53 decrease the expression of Mx1 but not weakened Jak2 phosphorylation.Cleaved Mdm2 might enhances the induction of p53 for innate cellular immunity.