Isolation of the YB strain of canine distemper virus from Yanbian, China: analysis of JAK2-STAT3 signaling and NLRP3 inflammasome activation in infected cells.

Canine distemper virus (CDV) is a highly contagious, multi-host pathogen that spreads readily among susceptible animals and often causes mass mortality. Yanbian Prefecture, located at the border area of China, Russia, and North Korea, represents a critical region for pathogen surveillance due to its unique geographical characteristics and animal trade activities; however, little is known about the prevalent CDV strains in this area or their pathogenic mechanisms. In this study, a CDV strain, designated CDV-Yanbian (CDV-YB), was successfully isolated from an anal swab sample collected from a suspected infected dog in Yanbian Prefecture and identified as the Asia-1 genotype through genetic analysis. To further elucidate the molecular mechanisms underlying CDV-host interactions, we examined the expression changes of inflammation-related signaling pathway genes and the occurrence of pyroptosis in canine adipose-derived mesenchymal stem cells (ADMSCs) following CDV infection using RT-qPCR and Western blot. Our results revealed that CDV infection activated the Janus kinase 2-Signal transducer and activator of transcription 3 (JAK2-STAT3), mitogen-activated protein kinase (MAPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathways and upregulated NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. Furthermore, inhibition of the JAK2-STAT3 pathway using AG490 reduced NLRP3 inflammasome activation. Taken together, our findings demonstrate that CDV activates multiple inflammatory signaling pathways and, via the JAK2-STAT3 pathway, upregulates NLRP3 inflammasome activation in host cells, and pyroptosis was also observed. These findings provide a foundation for understanding CDV pathogenesis and informing future research on this important virus.