Differential expression of type I interferon mRNA and protein levels induced by virulent Marek's disease virus infection in chickens

文献类型： 外文期刊

第一作者： Sun, Guo-rong

作者： Sun, Guo-rong;Zhou, Lin-yi;Zhang, Yan-ping;Zhang, Feng;Yu, Zheng-hao;Pan, Qing;Gao, Li;Li, Kai;Wang, Yong-qiang;Cui, Hong-yu;Qi, Xiaole;Gao, Yu-long;Wang, Xiao-mei;Liu, Chang-jun;Sun, Guo-rong;Zhou, Lin-yi;Zhang, Yan-ping;Zhang, Feng;Yu, Zheng-hao;Pan, Qing;Gao, Li;Li, Kai;Wang, Yong-qiang;Cui, Hong-yu;Qi, Xiaole;Gao, Yu-long;Wang, Xiao-mei;Liu, Chang-jun

作者机构：

关键词： Marek's disease virus; Innate immunity; Cytokine; Interferon

期刊名称：VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY （ 影响因子：2.046； 五年影响因子：2.217 ）

ISSN： 0165-2427

年卷期： 2019 年 212 卷

页码：

收录情况： SCI

摘要： Marek's disease virus (MDV), an alpha-herpesvirus targeting avian species, causes fatal Marek's disease (MD) in chickens. The host interferon (IFN) responses play a key role in resisting viral infection. However, host IFN responses following MDV infection in the chicken central immune organs (thymus and bursa of Fabricius), which contain numerous MDV target cells, is poorly understood. In this study, we performed animal experiments in specific pathogen-free chickens infected with two virulent MDV strains (BS/15 and Md5) or without infection as negative controls. Specifically, the type I IFN (IFN-alpha and IFN-beta) transcriptional and proteomic expression levels at 7, 10, 14, 17, and 21 days post infection (dpi) were detected and analyzed. Our results indicated that the mRNA and protein expression levels of IFN-alpha and IFN-beta in the thymus and bursa of Fabricius were mainly downregulated in cytolytic infection (such as 10 dpi) and reactivation (such as 17 dpi) stages, but not the latent (such as 14 dpi) stage of MDV infection, which was determined by comprehensively analyzing the MDV viral load and immune organ damage caused by MDV infection. These data suggest that MDV could inhibit the expression of host type I IFNs, which may be involved in the MDV-induced host immunosuppression and contribute to the immune escape of MDV from host immunity. Furthermore, we found that the downregulated expression of the host type I IFNs induced by BS/15 and Md5 infection was significantly different, which we speculated may be related to the diverse virulence and pathogenicity of MDV strains. In conclusion, our study demonstrated that MDV mostly inhibited the expression of type I IFNs in infected hosts, which may be associated to its pathogenesis.

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