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Microb Pathog ; 193: 106786, 2024 Aug.
Article de Anglais | MEDLINE | ID: mdl-38971506

RÉSUMÉ

To better understand the interaction between attenuated vaccines and host antiviral responses, we used bioinformatics and public transcriptomics data to analyze the immune response mechanisms of host cells after canine distemper virus (CDV) infection in Vero cells and screened for potential key effector factors. In this study, CDV-QN-1 infect with Vero cells at an MOI of 0.5, and total RNA was extracted from the cells 24 h later and reverse transcribed into cDNA. Transcriptome high-throughput sequencing perform using Illumina. The results showed that 438 differentially expressed genes were screened, of which 409 were significantly up-regulated and 29 were significantly down-regulated. Eight differentially expressed genes were randomly selected for RT-qPCR validation, and the change trend was consistent with the transcriptomics data. GO and KEGG analysis of differentially expressed genes revealed that most of the differentially expressed genes in CDV-QN-1 infection in the early stage were related to immune response and antiviral activity. The enriched signaling pathways mainly included the interaction between cytokines and cytokine receptors, the NF-kappa B signaling pathway, the Toll-like receptor signaling pathway, and the NOD-like receptor signaling pathway. This study provides a foundation for further exploring the pathogenesis of CDV and the innate immune response of host cells in the early stage of infection.


Sujet(s)
Virus de la maladie de Carré , Analyse de profil d'expression de gènes , Vaccins atténués , Animaux , Cellules Vero , Chlorocebus aethiops , Vaccins atténués/immunologie , Vaccins atténués/génétique , Virus de la maladie de Carré/génétique , Virus de la maladie de Carré/immunologie , Transcriptome , Transduction du signal , Biologie informatique , Séquençage nucléotidique à haut débit , Vaccins antiviraux/immunologie , Vaccins antiviraux/génétique , Cytokines/métabolisme , Cytokines/génétique , Maladie de Carré/virologie , Maladie de Carré/génétique , Maladie de Carré/immunologie , Interactions hôte-pathogène/génétique , Interactions hôte-pathogène/immunologie , Facteur de transcription NF-kappa B/métabolisme , Facteur de transcription NF-kappa B/génétique , Récepteurs de type Toll/génétique , Récepteurs de type Toll/métabolisme
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