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鸭肠炎病毒 VP16 拮抗 IFN--介导的抗病毒先天免疫。

Duck Enteritis Virus VP16 Antagonizes IFN--Mediated Antiviral Innate Immunity.

机构信息

Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Wenjiang 611130, China.

Avian Disease Research Center, College of Veterinary Medicine of Sichuan Agricultural University, Wenjiang 611130, China.

出版信息

J Immunol Res. 2020 May 15;2020:9630452. doi: 10.1155/2020/9630452. eCollection 2020.

DOI:10.1155/2020/9630452
PMID:32537474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7255046/
Abstract

Duck enteritis virus (DEV) can successfully evade the host innate immune responses and establish a lifelong latent infection in the infected host. However, the study about how DEV escapes host innate immunity is still deficient up to now. In this study, for the first time, we identified a viral protein VP16 by which DEV can obviously downregulate the production of IFN- in duck embryo fibroblast (DEF). Our results showed that ectopic expression of VP16 decreased duck IFN- (duIFN-) promoter activation and significantly inhibited the mRNA transcription of IFN-. Further study showed that VP16 can also obviously inhibit the mRNA transcription of interferon-stimulated genes (ISGs), such as myxovirus resistance protein (Mx) and interferon-induced oligoadenylate synthetase-like (OASL). Furthermore, we found that this anti-interferon activity of VP16 depended on its N-terminus (aa1-200). Coexpression analysis revealed that VP16 selectively blocked duIFN- promoter activity at the duIRF7 level rather than duIRF1. Based on the results of coimmunoprecipitation analysis (co-IP) and indirect immunofluorescence assay (IFA), VP16 was able to bind to duck IRF7 (duIRF7) directly, but did not interact with duck IRF1 (duIRF1) in vitro.

摘要

鸭肠炎病毒 (DEV) 能够成功逃避宿主固有免疫反应，并在受感染的宿主中建立终身潜伏感染。然而，到目前为止，关于 DEV 如何逃避宿主固有免疫的研究仍然不足。在这项研究中，我们首次鉴定了一种病毒蛋白 VP16，DEV 可以通过它明显地下调鸭胚成纤维细胞 (DEF) 中 IFN-的产生。我们的结果表明，VP16 的异位表达降低了鸭 IFN- (duIFN-) 启动子的激活，并显著抑制了 IFN-的 mRNA 转录。进一步的研究表明，VP16 还可以明显抑制干扰素刺激基因 (ISGs) 的 mRNA 转录，如抗黏液病毒蛋白 (Mx) 和干扰素诱导寡聚腺苷酸合成酶样 (OASL)。此外，我们发现 VP16 的这种抗病毒活性依赖于其 N 端 (aa1-200)。共表达分析表明，VP16 选择性地在 duIRF7 水平而非 duIRF1 水平阻断 duIFN-启动子活性。基于共免疫沉淀分析 (co-IP) 和间接免疫荧光分析 (IFA) 的结果，VP16 能够直接与鸭 IRF7 (duIRF7) 结合，但在体外不与鸭 IRF1 (duIRF1) 相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/320de78192b0/JIR2020-9630452.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/5ca98b8c76a4/JIR2020-9630452.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/b7b68e91a4b9/JIR2020-9630452.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/ea4ea773ea7c/JIR2020-9630452.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/241dc9629772/JIR2020-9630452.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/062f67ce16d1/JIR2020-9630452.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/320de78192b0/JIR2020-9630452.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/5ca98b8c76a4/JIR2020-9630452.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/b7b68e91a4b9/JIR2020-9630452.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/ea4ea773ea7c/JIR2020-9630452.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/241dc9629772/JIR2020-9630452.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/062f67ce16d1/JIR2020-9630452.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e12a/7255046/320de78192b0/JIR2020-9630452.006.jpg

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