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DEAD -box RNA 解旋酶 DDX1 与病毒蛋白 3D 相互作用并抑制口蹄疫病毒复制。

The DEAD-Box RNA Helicase DDX1 Interacts with the Viral Protein 3D and Inhibits Foot-and-Mouth Disease Virus Replication.

机构信息

Laboratory of Veterinary Microbiology, College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, 730070, China.

State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Diseases Reference Laboratory, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730046, China.

出版信息

Virol Sin. 2019 Dec;34(6):610-617. doi: 10.1007/s12250-019-00148-7. Epub 2019 Jul 29.

DOI:10.1007/s12250-019-00148-7
PMID:31359346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6888807/
Abstract

Foot-and-mouth disease virus (FMDV) can infect domestic and wild cloven-hoofed animals. The non-structural protein 3D plays an important role in FMDV replication and pathogenesis. However, the interaction partners of 3D, and the effects of those interactions on FMDV replication, remain incompletely elucidated. In the present study, using the yeast two-hybrid system, we identified a porcine cell protein, DEAD-box RNA helicase 1 (DDX1), which interacted with FMDV 3D. The DDX1-3D interaction was further confirmed by co-immunoprecipitation experiments and an indirect immunofluorescence assay (IFA) in porcine kidney 15 (PK-15) cells. DDX1 was reported to either inhibit or facilitate viral replication and regulate host innate immune responses. However, the roles of DDX1 during FMDV infection remain unclear. Our results revealed that DDX1 inhibited FMDV replication in an ATPase/helicase activity-dependent manner. In addition, DDX1 stimulated IFN-β activation in FMDV-infected cells. Together, our results expand the body of knowledge regarding the role of DDX1 in FMDV infection.

摘要

口蹄疫病毒(FMDV)可感染家养和野生偶蹄类动物。非结构蛋白 3D 在 FMDV 复制和发病机制中起重要作用。然而,3D 的相互作用伙伴以及这些相互作用对 FMDV 复制的影响仍不完全清楚。在本研究中,我们使用酵母双杂交系统鉴定了一种与 FMDV 3D 相互作用的猪细胞蛋白,即 DEAD 盒 RNA 解旋酶 1(DDX1)。DDX1-3D 相互作用通过共免疫沉淀实验和间接免疫荧光分析(IFA)在猪肾 15 (PK-15)细胞中进一步得到证实。DDX1 被报道可以抑制或促进病毒复制并调节宿主先天免疫反应。然而,DDX1 在 FMDV 感染过程中的作用尚不清楚。我们的研究结果表明,DDX1 以 ATPase/解旋酶活性依赖的方式抑制 FMDV 复制。此外,DDX1 刺激 FMDV 感染细胞中 IFN-β 的激活。总之,我们的研究结果扩展了 DDX1 在 FMDV 感染中的作用的知识体系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/1cbb0dfc2622/12250_2019_148_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/12f99a99cb84/12250_2019_148_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/5afcc60c2114/12250_2019_148_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/a25828ebd1be/12250_2019_148_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/14ca912783b1/12250_2019_148_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/1cbb0dfc2622/12250_2019_148_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/12f99a99cb84/12250_2019_148_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/5afcc60c2114/12250_2019_148_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/a25828ebd1be/12250_2019_148_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/14ca912783b1/12250_2019_148_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec1d/6888807/1cbb0dfc2622/12250_2019_148_Fig5_HTML.jpg

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3
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Virulence. 2024 Dec;15(1):2333562. doi: 10.1080/21505594.2024.2333562. Epub 2024 Apr 15.
4
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J Virol. 2023 Jun 29;97(6):e0049523. doi: 10.1128/jvi.00495-23. Epub 2023 Jun 8.
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7
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5
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8
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9
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10
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