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严重发热伴血小板减少综合征病毒 L 蛋白功能域和保守残基的作用为病毒 RNA 转录/复制机制提供了新见解。

Roles of the functional domains and conserved residues of the severe fever with thrombocytopenia syndrome virus L protein provide insights into the viral RNA transcription/replication mechanism.

机构信息

National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China; Academic Affairs Office of Cangzhou Jiaotong University, Cangzhou, 061199, China.

National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China; Center for Translational Medicine, Jinyintan Hospital, Wuhan, 430023, China.

出版信息

Virol Sin. 2022 Dec;37(6):946-949. doi: 10.1016/j.virs.2022.08.009. Epub 2022 Sep 3.

DOI:10.1016/j.virs.2022.08.009
PMID:36064095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9797366/
Abstract

• All the domains of SFTSV-L protein were required for its function in viral RNA replication/transcription. • The influence of twelve conserved residues were evaluated, nine of which showed significance in the function of L protein. • Nine residues of SFTSV-L were strictly conserved among phleboviruses, suggesting its potency as a promising drug target.

摘要

• SFTSV-L 蛋白的所有结构域均对其在病毒 RNA 复制/转录中的功能至关重要。

• 评估了十二个保守残基的影响，其中九个残基对 L 蛋白的功能具有重要意义。

• SFTSV-L 的九个残基在节肢动物病毒中严格保守，表明其作为有前途的药物靶标具有潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7161/9797366/0058bdc6edca/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7161/9797366/cef2e5aadab8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7161/9797366/0058bdc6edca/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7161/9797366/cef2e5aadab8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7161/9797366/0058bdc6edca/figs1.jpg

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本文引用的文献

1
Errors in the deposited SFTSV L protein structure.已存入的发热伴血小板减少综合征病毒L蛋白结构中的错误。
Nat Microbiol. 2021 May;6(5):549-550. doi: 10.1038/s41564-021-00901-3. Epub 2021 Apr 29.
2
Author Correction: Structure of severe fever with thrombocytopenia syndrome virus L protein elucidates the mechanisms of viral transcription initiation.作者更正：严重发热伴血小板减少综合征病毒L蛋白的结构揭示了病毒转录起始机制。
Nat Microbiol. 2021 May;6(5):697-698. doi: 10.1038/s41564-021-00906-y.
3
The Polarity of an Amino Acid at Position 1891 of Severe Fever with Thrombocytopenia Syndrome Virus L Protein Is Critical for the Polymerase Activity.
严重发热伴血小板减少综合征病毒 L 蛋白第 1891 位氨基酸的极性对聚合酶活性至关重要。
Viruses. 2020 Dec 27;13(1):33. doi: 10.3390/v13010033.
4
Structure of severe fever with thrombocytopenia syndrome virus L protein elucidates the mechanisms of viral transcription initiation.严重发热伴血小板减少综合征病毒 L 蛋白结构阐明了病毒转录起始的机制。
Nat Microbiol. 2020 Jun;5(6):864-871. doi: 10.1038/s41564-020-0712-2. Epub 2020 Apr 27.
5
Structural and functional characterization of the severe fever with thrombocytopenia syndrome virus L protein.严重发热伴血小板减少综合征病毒 L 蛋白的结构与功能特征。
Nucleic Acids Res. 2020 Jun 4;48(10):5749-5765. doi: 10.1093/nar/gkaa253.
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Heartland Virus Epidemiology, Vector Association, and Disease Potential.中心地带病毒的流行病学、媒介关联和疾病潜力。
Viruses. 2018 Sep 14;10(9):498. doi: 10.3390/v10090498.
7
A novel tick-borne phlebovirus, closely related to severe fever with thrombocytopenia syndrome virus and Heartland virus, is a potential pathogen.一种新型蜱传黄病毒，与发热伴血小板减少综合征病毒和 Heartland 病毒密切相关，是一种潜在的病原体。
Emerg Microbes Infect. 2018 May 25;7(1):95. doi: 10.1038/s41426-018-0093-2.
8
Hunter Island Group Phlebovirus in Ticks, Australia.澳大利亚蜱虫中的亨特岛群静脉病毒
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J Virol. 2014 Mar;88(6):3605-9. doi: 10.1128/JVI.02617-13. Epub 2014 Jan 3.