Isolation of the YB strain of canine distemper virus from Yanbian, China: analysis of JAK2-STAT3 signaling and NLRP3 inflammasome activation in infected cells.
Cao S., Ma H., Hao J., Ji X., Yu K., Zhang X.
Animal Study on Chronic Inflammation, published in J Vet Med Sci (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Vet Med Sci (2026)
- Country
- Japan
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42128845
- DOI
- 10.1292/jvms.26-0166
Abstract (original English)
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 acti
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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