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鱼类病毒性出血败血症病毒转录关闭的证据。

Evidence of Transcriptional Shutoff by Pathogenic Viral Haemorrhagic Septicaemia Virus in Rainbow Trout.

机构信息

International Centre of Excellence for Aquatic Animal Health, Cefas Weymouth Laboratory, Barrack Road, The Nothe, Weymouth DT4 8UB, Dorset, UK.

Biosciences, College of Life and Environmental Sciences, University of Exeter, Stocker Road, Exeter EX4 4QD, Devon, UK.

出版信息

Viruses. 2021 Jun 11;13(6):1129. doi: 10.3390/v13061129.

DOI:10.3390/v13061129
PMID:34208332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8231187/
Abstract

The basis of pathogenicity of viral haemorrhagic septicaemia virus (VHSV) was analysed in the transcriptome of a rainbow trout cell line inoculated with pathogenic and non-pathogenic VHSV isolates. Although both VHSV isolates showed similar viral replication patterns, the number of differentially expressed genes was 42-fold higher in cells inoculated with the non-pathogenic VHSV at 3 h post inoculation (hpi). Infection with the non-pathogenic isolate resulted in Gene Ontologies (GO) enrichment of terms such as immune response, cytokine-mediated signalling pathway, regulation of translational initiation, unfolded protein binding, and protein folding, and induced an over-representation of the p53, PPAR, and TGF-β signalling pathways. Inoculation with the pathogenic isolate resulted in the GO enrichment of terms related to lipid metabolism and the salmonella infection KEGG pathway involved in the rearrangement of the cytoskeleton. Antiviral response was evident at 12hpi in cells infected with the pathogenic isolate. Overall, the data showed a delay in the response of genes involved in immune responses and viral sensing in cells inoculated with the pathogenic isolate and suggest transcriptional shutoff and immune avoidance as a critical mechanism of pathogenicity in VHSV. These pathways offer opportunities to further understand and manage VHSV pathogenicity in rainbow trout.

摘要

病毒性出血性败血症病毒 (VHSV) 的致病性基础在接种致病性和非致病性 VHSV 分离株的虹鳟鱼细胞系的转录组中进行了分析。尽管两种 VHSV 分离株的病毒复制模式相似,但在接种非致病性 VHSV 后 3 小时(hpi),差异表达基因的数量高出 42 倍。非致病性分离株的感染导致了与免疫反应、细胞因子介导的信号通路、翻译起始的调节、未折叠蛋白结合和蛋白质折叠等相关的基因本体论 (GO) 富集,并且诱导了 p53、PPAR 和 TGF-β 信号通路的过度表达。接种致病性分离株导致与脂质代谢相关的 GO 富集和涉及细胞骨架重排的沙门氏菌感染 KEGG 途径。在接种致病性分离株的细胞中,在 12 hpi 时出现了抗病毒反应。总的来说,数据表明,接种致病性分离株的细胞中,参与免疫反应和病毒感应的基因的反应延迟,并表明转录关闭和免疫逃避是 VHSV 致病性的关键机制。这些途径为进一步了解和管理虹鳟鱼 VHSV 的致病性提供了机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/647e33b47198/viruses-13-01129-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/de49a1428097/viruses-13-01129-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/c552671eb39e/viruses-13-01129-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/5be100624e40/viruses-13-01129-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/a62f11ccb6d3/viruses-13-01129-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/647e33b47198/viruses-13-01129-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/de49a1428097/viruses-13-01129-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/c552671eb39e/viruses-13-01129-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/5be100624e40/viruses-13-01129-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/a62f11ccb6d3/viruses-13-01129-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90aa/8231187/647e33b47198/viruses-13-01129-g005.jpg

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