Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins
Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins
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DOI：
10.1101/cshperspect.a038307
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发表时间：
2021-11-01
影响因子：
5.4
通讯作者：
Barclay，Wendy S.
中科院分区：
文献类型：
--
作者：
Staller，Ecco;Barclay，Wendy S.
流感病毒在病毒生命周期的每个阶段劫持宿主细胞因子。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，在细胞质中经典的细胞核输入途径被篡夺用于vRNP的核易位。转录发生在细胞核内活跃的宿主转录位点，并且细胞mRNA输出途径被破坏以输出病毒mRNA。新合成的RNP组分使用各种细胞核输入途径和宿主编码的分子伴侣循环回到细胞核中。负义病毒RNA（vRNA）复制成互补RNA（cRNA）并复制回vRNA需要病毒和宿主因子之间复杂的相互作用。子代vRNP在宿主染色质处组装，随后从由宿主和病毒蛋白质组编排的核过程中退出。最后，几种宿主途径似乎在vRNP从核膜到质膜的运输中起作用。
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.