Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Ave, Los Angeles, CA, 90089, USA.
Graduate School of Health and Sports Science, Juntendo University, Chiba, Japan.
Sci Rep. 2021 Jan 8;11(1):3. doi: 10.1038/s41598-020-79552-z.
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.
与其他呼吸道病毒相比，SARS-CoV-2 诱导的先天免疫反应较弱。线粒体动力学可能部分介导了 SARS-CoV-2 对先天免疫的这种影响。已表明 SARS-CoV 和 SARS-CoV-2 的开放阅读框编码的多肽定位于线粒体，并破坏线粒体抗病毒信号（MAVS）蛋白信号。因此，我们假设 SARS-CoV-2 将明显调节线粒体转录组。我们分析了来自原代细胞、细胞系和临床样本（即 BALF 和肺）的多个公开可用的 RNA-Seq 数据。我们报告说，SARS-CoV-2 并没有显著调节（1）mtDNA 编码基因的表达或（2）MAVS 的表达，并且（3）SARS-CoV-2 下调了与细胞呼吸和复合物 I 相关的核编码线粒体（NEM）基因。
