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《Antiviral Research，3月1日，A potential role for integrins in host cell entry by SARS-CoV-2》

  • 来源专题：COVID-19科研动态监测
  • 编译者： zhangmin
  • 发布时间：2020-03-02

  • A potential role for integrins in host cell entry by SARS-CoV-2

    ChristianSigrist, AlanBridge, PhilippeLe Mercier

    https://doi.org/10.1016/j.antiviral.2020.104759

    Since December 2019, a novel coronavirus (nCoV) of animal origin started infecting humans, initiating a severe outbreak in China. This virus, named “Severe Acute Respiratory Syndrome-related Coronavirus 2” (SARS-CoV-2), can cause a severe and even fatal respiratory disease, called Coronavirus disease-19 (COVID-19), and lead to acute respiratory distress syndrome (ARDS). The virus is highly contagious and transmission occurs presumably via airborne droplets, and fecal-oral route (Zhang et al., 2020).

  • 原文来源：https://www.sciencedirect.com/science/article/pii/S0166354220300929
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    • 来源专题：COVID-19科研动态监测
    • 编译者：zhangmin
    • 发布时间：2021-03-29
    • SARS-CoV-2 infection rewires host cell metabolism and is potentially susceptible to mTORC1 inhibition Peter J. Mullen, Gustavo Garcia Jr, Arunima Purkayastha, Nedas Matulionis, Ernst W. Schmid, Milica Momcilovic, Chandani Sen, Justin Langerman, Arunachalam Ramaiah, David B. Shackelford, Robert Damoiseaux, Samuel W. French, Kathrin Plath, Brigitte N. Gomperts, Vaithilingaraja Arumugaswami & Heather R. Christofk Nature Communications volume 12, Article number: 1876 (2021) Abstract Viruses hijack host cell metabolism to acquire the building blocks required for replication. Understanding how SARS-CoV-2 alters host cell metabolism may lead to potential treatments for COVID-19. Here we profile metabolic changes conferred by SARS-CoV-2 infection in kidney epithelial cells and lung air-liquid interface (ALI) cultures, and show that SARS-CoV-2 infection increases glucose carbon entry into the TCA cycle via increased pyruvate carboxylase expression. SARS-CoV-2 also reduces oxidative glutamine metabolism while maintaining reductive carboxylation. Consistent with these changes, SARS-CoV-2 infection increases the activity of mTORC1 in cell lines and lung ALI cultures. Lastly, we show evidence of mTORC1 activation in COVID-19 patient lung tissue, and that mTORC1 inhibitors reduce viral replication in kidney epithelial cells and lung ALI cultures. Our results suggest that targeting mTORC1 may be a feasible treatment strategy for COVID-19 patients, although further studies are required to determine the mechanism of inhibition and potential efficacy in patients.
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  • 《3月1日_整合素在SARS-CoV-2进入宿主细胞中的潜在作用》
    • 来源专题：COVID-19科研动态监测
    • 编译者：zhangmin
    • 发布时间：2020-03-02
    • 1.时间：2020年3月1日 2.信息来源：Antiviral Research 3.机构或团队：瑞士生物信息学研究所 4.事件概要： 瑞士生物信息学研究所在Antiviral Research发表论文“A potential role for integrins in host cell entry by SARS-CoV-2”。 作者认为SARS-CoV-2可以通过刺突蛋白（S）中RGD保守序列部分结合到宿主细胞整合素上，从而进入宿主细胞。RGD序列是结合整合素家族所需的最小肽序列，PROSITE筛选结果显示该序列在其他冠状病毒（包括SARS）中没有出现。文章猜测病毒与整合素的结合可能对ACE2结合起补充作用，如通过整合素发出的信号促进内吞，也可能是病毒分别通过与ACE2或整合素结合感染不同的细胞，相关机制还有待进一步研究。 5.附件： 原文链接： https://www.sciencedirect.com/science/article/pii/S0166354220300929
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