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抗病毒感知和I型干扰素信号在限制SARS-CoV-2复制中的作用。

Roles of antiviral sensing and type I interferon signaling in the restriction of SARS-CoV-2 replication.

作者信息

Geerling Elizabeth, Pinski Amanda N, Stone Taylor E, DiPaolo Richard J, Zulu Michael Z, Maroney Kevin J, Brien James D, Messaoudi Ilhem, Pinto Amelia K

机构信息

Department of Molecular Microbiology and Immunology, Saint Louis University, St Louis, MO 63103, USA.

Department of Molecular Biology and Biochemistry, University of California-Irvine, Irvine, CA 92697, USA.

出版信息

iScience. 2022 Jan 21;25(1):103553. doi: 10.1016/j.isci.2021.103553. Epub 2021 Dec 3.

DOI:10.1016/j.isci.2021.103553
PMID:34877479
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8639477/
Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019. Few studies have compared replication dynamics and host responses to SARS-CoV-2 in cell lines from different tissues and species. Therefore, we investigated the role of tissue type and antiviral genes during SARS-CoV-2 infection in nonhuman primate (kidney) and human (liver, respiratory epithelial, gastric) cell lines. We report different viral growth kinetics and release among the cell lines despite comparable ACE2 expression. Transcriptomics revealed that absence of in nonhuman primate cells appeared to enhance inflammatory responses without effecting infectious viral titer. Deletion of in respiratory epithelial cells increased viral replication. Impaired infectious virus release was detected in Huh7 but not Huh7.5 cells, suggesting a role for . Gastric cells MKN45 exhibited robust antiviral gene expression and supported viral replication. Data here provide insight into molecular pathogenesis of and alternative cell lines for studying SARS-CoV-2 infection.

摘要

严重急性呼吸综合征冠状病毒2(SARS-CoV-2)是2019冠状病毒病的病原体。很少有研究比较不同组织和物种的细胞系中SARS-CoV-2的复制动力学和宿主反应。因此,我们研究了组织类型和抗病毒基因在非人类灵长类动物(肾脏)和人类(肝脏、呼吸道上皮、胃)细胞系感染SARS-CoV-2过程中的作用。我们报告了尽管ACE2表达相当,但各细胞系之间的病毒生长动力学和释放情况不同。转录组学显示,非人类灵长类动物细胞中缺乏 似乎增强了炎症反应,而不影响感染性病毒滴度。呼吸道上皮细胞中 的缺失增加了病毒复制。在Huh7细胞中检测到感染性病毒释放受损,但在Huh7.5细胞中未检测到,这表明 起了作用。胃细胞MKN45表现出强大的抗病毒基因表达并支持病毒复制。此处的数据为研究SARS-CoV-2感染的分子发病机制和替代细胞系提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/3428baf6e597/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/15985a77c46d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/a01361313d6d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/5919ae58e265/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/a3295c37448d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/c68d5521d5f5/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/3428baf6e597/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/15985a77c46d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/a01361313d6d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/5919ae58e265/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/a3295c37448d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/c68d5521d5f5/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18e0/8689155/3428baf6e597/gr5.jpg

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