Transcriptome analysis of senecavirus A-infected cells: Type I interferon is a critical anti-viral factor. (October 2020)

• Record Type: Journal Article
• Authors: Wang, Jing; Mou, Chunxiao; Wang, Minmin; Pan, Shuonan; Chen, Zhenhai
• Is Part Of: Microbial pathogenesis. Volume 147(2020)
• Publication Date: 2020-10
• Subjects: Senecavirus A -- Vesicular disease -- Gene expression profile -- Innate immune -- Type I IFN; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2020.104432
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Senecavirus A (SVA)-associated vesicular disease (SAVD) has extensively been present in the swine industry during the past years. The mechanisms of SVA-host interactions at the molecular level, subsequent to SVA infection, are unclear. We studied the gene expression profiles of LLC-PK1 cells, with or without SVA infection, for 6 h and 12 h using an RNA-seq technology. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on differentially expressed genes (DEGs). Immune-related genes and pathways were significantly modified after SVA infection. To confirm the RNA-seq data, 28 important DEGs were selected for RT-qPCR assays. All DEGs exhibited expression patterns consistent with the RNA-seq results. Among them, type I IFNs (including IFN-α and IFN-β) showed the largest upregulation, followed by RSAD2, DDX58, MX1 and the 17 other DEGs. In contrary, ID2 and another 5 DEGs were down-regulated or unchanged. These results indicated that type I IFNs play a critical role in host immune responses against SVA infection at early stage, while other immune-regulated genes directly or indirectly participate in the host immune responses. Highlights: Senecavirus A (SVA) is the causative agent of SVA-associated vesicular disease (SAVD). A global change of host cell gene expression after SVA infection. 294 pathways were enriched at 6hpi and 305 were enriched at 12hpi. Type I IFNs play a critical role in host defense against SVA infection. RSAD2, DDX58, MX1, TNF-α etc. appear to work in defense against SVA.