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与流感病毒核糖核蛋白相互作用的宿主细胞因子。

Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins.

机构信息

Department of Infectious Disease, Faculty of Medicine, Imperial College London, St. Mary's Campus, London W2 1NY, United Kingdom.

出版信息

Cold Spring Harb Perspect Med. 2021 Nov 1;11(11):a038307. doi: 10.1101/cshperspect.a038307.

Abstract

Influenza viruses hijack host cell factors at each stage of the viral life cycle. After host cell entry and endosomal escape, the influenza viral ribonucleoproteins (vRNPs) are released into the cytoplasm where the classical cellular nuclear import pathway is usurped for nuclear translocation of the vRNPs. Transcription takes place inside the nucleus at active host transcription sites, and cellular mRNA export pathways are subverted for export of viral mRNAs. Newly synthesized RNP components cycle back into the nucleus using various cellular nuclear import pathways and host-encoded chaperones. Replication of the negative-sense viral RNA (vRNA) into complementary RNA (cRNA) and back into vRNA requires complex interplay between viral and host factors. Progeny vRNPs assemble at the host chromatin and subsequently exit from the nucleus-processes orchestrated by sets of host and viral proteins. Finally, several host pathways appear to play a role in vRNP trafficking from the nuclear envelope to the plasma membrane for egress.

摘要

流感病毒在病毒生命周期的每个阶段都会劫持宿主细胞因子。在宿主细胞进入和内体逃逸后,流感病毒核糖核蛋白(vRNP)被释放到细胞质中,经典的细胞核输入途径被劫持用于 vRNP 的核易位。转录发生在活跃的宿主转录位点的细胞核内,细胞 mRNA 输出途径被颠覆以输出病毒 mRNAs。新合成的 RNP 组件使用各种细胞核输入途径和宿主编码的伴侣蛋白循环回到细胞核。负义病毒 RNA(vRNA)复制成互补 RNA(cRNA)并再回到 vRNA 需要病毒和宿主因子之间的复杂相互作用。子代 vRNP 在宿主染色质上组装,然后从细胞核中输出——这一过程由一组宿主和病毒蛋白协调。最后,一些宿主途径似乎在 vRNP 从核膜到质膜的运输中发挥作用,以实现出芽。

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