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一种融合性蝙蝠源性呼肠孤病毒的非结构蛋白 p17 以病毒种属和宿主特异性的方式调节病毒复制。

The nonstructural p17 protein of a fusogenic bat-borne reovirus regulates viral replication in virus species- and host-specific manners.

机构信息

Department of Virology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.

Special Pathogens Laboratory, Department of Virology I, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan.

出版信息

PLoS Pathog. 2022 Jun 2;18(6):e1010553. doi: 10.1371/journal.ppat.1010553. eCollection 2022 Jun.

DOI:10.1371/journal.ppat.1010553
PMID:35653397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9162341/
Abstract

Nelson Bay orthoreovirus (NBV), a member of the family Reoviridae, genus Orthoreovirus, is a bat-borne virus that causes respiratory diseases in humans. NBV encodes two unique nonstructural proteins, fusion-associated small transmembrane (FAST) protein and p17 protein, in the S1 gene segment. FAST induces cell-cell fusion between infected cells and neighboring cells and the fusogenic activity is required for efficient viral replication. However, the function of p17 in the virus cycle is not fully understood. Here, various p17 mutant viruses including p17-deficient viruses were generated by a reverse genetics system for NBV. The results demonstrated that p17 is not essential for viral replication and does not play an important role in viral pathogenesis. On the other hand, NBV p17 regulated viral replication in a bat cell line but not in other human and animal cell lines. Nuclear localization of p17 is associated with the regulation of NBV replication in bat cells. We also found that p17 dramatically enhances the cell-cell fusion activity of NBV FAST protein for efficient replication in bat cells. Furthermore, we found that a protein homologue of NBV p17 from another bat-borne orthoreovirus, but not those of avian orthoreovirus or baboon orthoreovirus, also supported efficient viral replication in bat cells using a p17-deficient virus-based complementation approach. These results provide critical insights into the functioning of the unique replication machinery of bat-borne viruses in their natural hosts.

摘要

尼尔森湾正呼肠孤病毒（NBV），呼肠孤病毒科，正呼肠孤病毒属的一种病毒，是一种能感染蝙蝠并导致人类呼吸道疾病的病毒。NBV 在 S1 基因片段中编码两种独特的非结构蛋白，融合相关小跨膜（FAST）蛋白和 p17 蛋白。FAST 诱导感染细胞与邻近细胞之间的细胞-细胞融合，其融合活性是病毒高效复制所必需的。然而，p17 在病毒周期中的功能尚未完全阐明。在这里，我们使用 NBV 的反向遗传学系统生成了各种 p17 突变病毒，包括 p17 缺失病毒。结果表明，p17 对于病毒复制不是必需的，在病毒发病机制中也不起重要作用。另一方面，NBV p17 在蝙蝠细胞系中调节病毒复制，但在其他人和动物细胞系中没有作用。p17 的核定位与在蝙蝠细胞中调节 NBV 复制有关。我们还发现，p17 极大地增强了 NBV FAST 蛋白的细胞-细胞融合活性，有利于在蝙蝠细胞中的高效复制。此外，我们发现，来自另一种蝙蝠携带的正呼肠孤病毒的 NBV p17 的蛋白同源物，但不是禽正呼肠孤病毒或狒狒正呼肠孤病毒的蛋白同源物，也通过使用 p17 缺失病毒的互补方法支持蝙蝠细胞中的病毒有效复制。这些结果为蝙蝠携带病毒在其自然宿主中的独特复制机制的功能提供了重要的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/0d702d071e48/ppat.1010553.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/04e1ecb88d2f/ppat.1010553.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/ae337d348bb2/ppat.1010553.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/f0b009cbdf7d/ppat.1010553.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/d4e1ab721e8d/ppat.1010553.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/f4a3807aea0c/ppat.1010553.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/1f0152fd9a8a/ppat.1010553.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/89f75b35be33/ppat.1010553.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/e0cb98b15997/ppat.1010553.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/0d702d071e48/ppat.1010553.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/04e1ecb88d2f/ppat.1010553.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/ae337d348bb2/ppat.1010553.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/f0b009cbdf7d/ppat.1010553.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/d4e1ab721e8d/ppat.1010553.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/f4a3807aea0c/ppat.1010553.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/1f0152fd9a8a/ppat.1010553.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/89f75b35be33/ppat.1010553.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/e0cb98b15997/ppat.1010553.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c37a/9162341/0d702d071e48/ppat.1010553.g009.jpg

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