Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.

Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.
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DOI:
10.1038/s41598-020-79552-z
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发表时间:
2021-01-08
期刊:
影响因子:
4.6
通讯作者:
Cohen P
Cohen P
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Miller B;Silverstein A;Flores M;Cao K;Kumagai H;Mehta HH;Yen K;Kim SJ;Cohen P

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与其他呼吸道病毒相比,SARS-CoV-2诱导了一种温和的先天免疫反应。线粒体动力学可能部分介导了SARS-CoV-2对先天免疫的影响。由SARS-CoV和SARS-CoV-2的开放阅读框编码的多肽已显示定位于线粒体并破坏线粒体抗病毒信号传导(MAVS)蛋白信号传导。因此,我们假设SARS-CoV-2将明显调节线粒体转录组。我们分析了来源于原代细胞、细胞系和临床样品(即,BALF和肺)。我们报告SARS-CoV-2没有显著调节(1)mtDNA编码的基因表达或(2)MAVS表达,(3)SARS-CoV-2下调与细胞呼吸和复合体I相关的核编码线粒体(NEM)基因。
SARS-CoV-2 induces a muted innate immune response compared to other respiratory viruses. Mitochondrial dynamics might partially mediate this effect of SARS-CoV-2 on innate immunity. Polypeptides encoded by open reading frames of SARS-CoV and SARS-CoV-2 have been shown to localize to mitochondria and disrupt Mitochondrial Antiviral Signaling (MAVS) protein signaling. Therefore, we hypothesized that SARS-CoV-2 would distinctly regulate the mitochondrial transcriptome. We analyzed multiple publicly available RNASeq data derived from primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report that SARS-CoV-2 did not dramatically regulate (1) mtDNA-encoded gene expression or (2) MAVS expression, and (3) SARS-CoV-2 downregulated nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex I.
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