Ursodeoxycholic acid inhibits feline infectious peritonitis virus infection through activating JAK-STAT signaling pathway-induced type I interferon

culture of FIPV, but also lays a theoretical foundation for the development of anti-FIPV drugs targeting the JAK-STAT pathway. IMPORTANCE: In this study, through the establishment of a complete research chain of "virus titer-enhanced cell model-drug effect evaluation-signaling pathway analysis", we confirmed that ursodeoxycholic acid (UDCA) can inhibit feline infectious peritonitis virus (FIPV) infection and revealed that UDCA can activate the JAK-STAT signaling pathway by promoting the production of large amounts of interferon-β in host cells to protect against FIPV infection. It not only provides a new experimental tool (CRFK-PHBLV-N cell line) and drug candidate (UDCA) for FIP prevention and control, but also lays a theoretical foundation for the development of novel therapeutic strategies targeting the host antiviral pathway through the elucidation of the JAK-STAT pathway mechanism.