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The host transcriptome change involved in the inhibitory effect of exogenous interferon-& gamma; on Getah virus replication

文献类型： 外文期刊

作者： Li, Jialei;Gao, Xintao;Liu, Xingjian;Wu, Tong;Song, Haozhi;Gao, Weisong;Jia, Hong;Li, Yinue;Zhang, Zhifang

作者机构：

关键词： Getah virus;immune escape;IFN-& gamma;inhibition of replication;transcriptome change

期刊名称： FRONTIERS IN MICROBIOLOGY

ISSN：

年卷期： 2023 年 14 卷

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收录情况： SCIE（2023版）

摘要： Introduction: Getah virus (GETV) has become a growing potential threat to the global livestock industry and public health. However, little is known about the viral pathogenesis and immune escape mechanisms, leading to ineffective control measures.Methods: In this study, the antiviral activity of exogenous interferons (IFNs) was assessed by using western blotting (WB), real-time quantitative PCR (RT-qPCR) and indirect immunofluorescence assay (IFA). The comparative transcriptomics among mock- and GETV-infected (MOI = 0.1) ST cells with or without IFN-? was performed by RNA-seq, and then the transcriptome profiling of GETV-infected ST cells and key pathways and putative factors involved in inhibitory effect of IFN-? on GETV replication were analyzed by bioinformatics methods and RT-qPCR.Results: The results showed that treatment with IFN-? could suppress GETV replication, and the inhibitory effect lasted for at least 48 h, while the exogenous IFN-a/? and IFN-?3 treatments failed to inhibit the viral infection and early replication in vitro. Furthermore, the blueprint of virus-host interaction was plotted by RNA-seq and RT-qPCR, showing systemic activation of inflammatory, apoptotic, and antiviral pathways in response to GETV infection, indicating viral hijacking and inhibition of innate host immunity such as IFN-I/III responses. Last and most importantly, activation of the JAK-STAT signaling pathway and complement and coagulation cascades may be a primary driver for IFN-?-mediated inhibition of GETV replication.Discussion: These findings revealed that GETV possessed the capability of viral immune escape and indicated that IFN-? aided in the prevention and control of GETV, implying the potential molecular mechanism of suppression of GETV by IFN-?, all of which warrant emphasis or further clarification.

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