RNA sequencing analyses of gene expressions in a canine macrophages cell line DH82 infected with canine distemper virus

文献类型： 外文期刊

第一作者： Zheng, Xuexing

作者： Zheng, Xuexing;Zhu, Yelei;Zhao, Zhongxin;Yan, Lina;Xu, Tong;Zheng, Wenwen;Xue, Xianghong;Zhu, Yelei;Wang, Xianwei;He, Hongbin;Xia, Xianzhu

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关键词： Canine distemper virus; Antiviral responses; Macrophages; Transcriptomic; Differentially expression genes

期刊名称：INFECTION GENETICS AND EVOLUTION （ 影响因子：3.342； 五年影响因子：3.188 ）

ISSN： 1567-1348

年卷期： 2020 年 80 卷

页码：

收录情况： SCI

摘要： Virulent morbillivirus infections, including Meals Virus (MeV) and Canine Distemper Virus (CDV), caused severe immune suppression and leukopenia, while attenuated vaccine strains developed protective host immune responses. However, the detailed molecular foundations of host antiviral responses were poorly characterized. In order to better understand the interactions between attenuated vaccine and host antiviral responses, the global gene expression changes in CDV-11-infected DH82 cells, a macrophage-derived cell line from canine, were investigated by transcriptomic analysis, and portions of results were confirmed with quantitative RT-PCR. The results exhibited that 372 genes significantly up-regulated (p < .01) and 119 genes were significantly down-regulated (p < .01) in CDV-infected macrophages DH82 at 48 h p.i.. The enriched functions of the significantly up-regulated (p < .01) genes were closely associated with interferon stimulated genes (ISGs), chemokine genes and pro-inflammatory factor genes. Gene ontology and pathway analysis of differentially expressed genes (DEGs) revealed that the most significantly involved pathways in CDV-infected DH82 cells were NF-kappa B and TNF signaling pathway, cytokine-cytokine receptor interaction, and pathogen associated molecular patterns (PAMPs), such as Toll-like, RIG-I-like and NOD-like receptor signalings. Thus, the findings indicated that pattern recognition receptors (PRRs) possibly mediated host innate and protective antiviral immune responses in CDV-11 infected DH82 cells.

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