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H9N2 病毒衍生的 M1 蛋白促进哺乳动物细胞中 H5N6 病毒的释放：人类中禽流感病毒种间感染的机制。

H9N2 virus-derived M1 protein promotes H5N6 virus release in mammalian cells: Mechanism of avian influenza virus inter-species infection in humans.

机构信息

Key Laboratory of Animal Epidemiology, Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing, China.

School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, United Kingdom.

出版信息

PLoS Pathog. 2021 Dec 3;17(12):e1010098. doi: 10.1371/journal.ppat.1010098. eCollection 2021 Dec.

DOI:10.1371/journal.ppat.1010098
PMID:34860863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8641880/
Abstract

H5N6 highly pathogenic avian influenza virus (HPAIV) clade 2.3.4.4 not only exhibits unprecedented intercontinental spread in poultry, but can also cause serious infection in humans, posing a public health threat. Phylogenetic analyses show that 40% (8/20) of H5N6 viruses that infected humans carried H9N2 virus-derived internal genes. However, the precise contribution of H9N2 virus-derived internal genes to H5N6 virus infection in humans is unclear. Here, we report on the functional contribution of the H9N2 virus-derived matrix protein 1 (M1) to enhanced H5N6 virus replication capacity in mammalian cells. Unlike H5N1 virus-derived M1 protein, H9N2 virus-derived M1 protein showed high binding affinity for H5N6 hemagglutinin (HA) protein and increased viral progeny particle release in different mammalian cell lines. Human host factor, G protein subunit beta 1 (GNB1), exhibited strong binding to H9N2 virus-derived M1 protein to facilitate M1 transport to budding sites at the cell membrane. GNB1 knockdown inhibited the interaction between H9N2 virus-derived M1 and HA protein, and reduced influenza virus-like particles (VLPs) release. Our findings indicate that H9N2 virus-derived M1 protein promotes avian H5N6 influenza virus release from mammalian, in particular human cells, which could be a major viral factor for H5N6 virus cross-species infection.

摘要

H5N6 高致病性禽流感病毒（HPAIV） 2.3.4.4 分支不仅在禽类中表现出前所未有的洲际传播，还能导致人类严重感染，对公共卫生构成威胁。系统进化分析表明，感染人类的 40%（8/20）H5N6 病毒携带 H9N2 病毒衍生的内部基因。然而，H9N2 病毒衍生的内部基因对 H5N6 病毒感染人类的确切贡献尚不清楚。在这里，我们报告了 H9N2 病毒衍生的基质蛋白 1（M1）对增强 H5N6 病毒在哺乳动物细胞中的复制能力的功能贡献。与 H5N1 病毒衍生的 M1 蛋白不同，H9N2 病毒衍生的 M1 蛋白对 H5N6 血凝素（HA）蛋白具有高结合亲和力，并增加了不同哺乳动物细胞系中的病毒子代颗粒释放。人类宿主因子 G 蛋白亚基β1（GNB1）与 H9N2 病毒衍生的 M1 蛋白具有很强的结合能力，有助于 M1 蛋白向细胞膜出芽部位转运。GNB1 敲低抑制了 H9N2 病毒衍生的 M1 与 HA 蛋白之间的相互作用，并减少了流感病毒样颗粒（VLPs）的释放。我们的研究结果表明，H9N2 病毒衍生的 M1 蛋白促进了禽源 H5N6 流感病毒从哺乳动物，特别是人类细胞中的释放，这可能是 H5N6 病毒跨种感染的主要病毒因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/cc1f3f67ad37/ppat.1010098.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/94a4f9e7d7cf/ppat.1010098.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/b4044ed8b00b/ppat.1010098.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/6e63e0b4dd87/ppat.1010098.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/6bda80d7eff6/ppat.1010098.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/020d3148aaf3/ppat.1010098.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/42cd3c5f3b58/ppat.1010098.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/c5122a00fe3a/ppat.1010098.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/5376d48024e0/ppat.1010098.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/cc1f3f67ad37/ppat.1010098.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/94a4f9e7d7cf/ppat.1010098.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/b4044ed8b00b/ppat.1010098.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/6e63e0b4dd87/ppat.1010098.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/6bda80d7eff6/ppat.1010098.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/020d3148aaf3/ppat.1010098.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/42cd3c5f3b58/ppat.1010098.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/c5122a00fe3a/ppat.1010098.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/5376d48024e0/ppat.1010098.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f8a/8641880/cc1f3f67ad37/ppat.1010098.g009.jpg

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