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大西洋鲑血细胞中鱼正呼肠孤病毒感染的病毒蛋白动力学

Viral Protein Kinetics of Piscine Orthoreovirus Infection in Atlantic Salmon Blood Cells.

作者信息

Haatveit Hanne Merethe, Wessel Øystein, Markussen Turhan, Lund Morten, Thiede Bernd, Nyman Ingvild Berg, Braaen Stine, Dahle Maria Krudtaa, Rimstad Espen

机构信息

Department of Food Safety and Infectious Biology, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, 0454 Oslo, Norway.

Department of Immunology, Norwegian Veterinary Institute, 0454 Oslo, Norway.

出版信息

Viruses. 2017 Mar 18;9(3):49. doi: 10.3390/v9030049.

DOI:10.3390/v9030049
PMID:28335455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5371804/
Abstract

(PRV) is ubiquitous in farmed Atlantic salmon () and the cause of heart and skeletal muscle inflammation. Erythrocytes are important target cells for PRV. We have investigated the kinetics of PRV infection in salmon blood cells. The findings indicate that PRV causes an acute infection of blood cells lasting 1-2 weeks, before it subsides into persistence. A high production of viral proteins occurred initially in the acute phase which significantly correlated with antiviral gene transcription. Globular viral factories organized by the non-structural protein µNS were also observed initially, but were not evident at later stages. Interactions between µNS and the PRV structural proteins λ1, µ1, σ1 and σ3 were demonstrated. Different size variants of µNS and the outer capsid protein µ1 appeared at specific time points during infection. Maximal viral protein load was observed five weeks post cohabitant challenge and was undetectable from seven weeks post challenge. In contrast, viral RNA at a high level could be detected throughout the eight-week trial. A proteolytic cleavage fragment of the µ1 protein was the only viral protein detectable after seven weeks post challenge, indicating that this µ1 fragment may be involved in the mechanisms of persistent infection.

摘要

传染性胰腺坏死病毒(PRV)在养殖的大西洋鲑鱼中普遍存在,是心脏和骨骼肌炎症的病因。红细胞是PRV的重要靶细胞。我们研究了PRV在鲑鱼血细胞中的感染动力学。研究结果表明,PRV会引起血细胞的急性感染,持续1至2周,之后进入持续感染状态。病毒蛋白的大量产生最初发生在急性期,这与抗病毒基因转录显著相关。最初还观察到由非结构蛋白µNS组织形成的球状病毒工厂,但在后期并不明显。证实了µNS与PRV结构蛋白λ1、µ1、σ1和σ3之间存在相互作用。在感染期间的特定时间点出现了不同大小变体的µNS和外衣壳蛋白µ1。在同居挑战后五周观察到最大病毒蛋白载量,在挑战后七周检测不到。相比之下,在整个八周试验中都能检测到高水平的病毒RNA。µ1蛋白的一个蛋白水解裂解片段是挑战后七周唯一可检测到的病毒蛋白,表明该µ1片段可能参与持续感染机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/445236719dd8/viruses-09-00049-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/d94279b62581/viruses-09-00049-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/a2fca2454a57/viruses-09-00049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/ba073dd0586a/viruses-09-00049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/4bf1524c8aaf/viruses-09-00049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/6ba25bf5359c/viruses-09-00049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/b5a0e7614603/viruses-09-00049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/445236719dd8/viruses-09-00049-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/d94279b62581/viruses-09-00049-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/a2fca2454a57/viruses-09-00049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/ba073dd0586a/viruses-09-00049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/4bf1524c8aaf/viruses-09-00049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/6ba25bf5359c/viruses-09-00049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/b5a0e7614603/viruses-09-00049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0591/5371804/445236719dd8/viruses-09-00049-g007.jpg

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