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利用公开的冠状病毒数据为 COVID-19 确定新的治疗靶点。

Leveraging publicly available coronavirus data to identify new therapeutic targets for COVID-19.

机构信息

Department of Anesthesiology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.

Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.

出版信息

PLoS One. 2021 Sep 29;16(9):e0257965. doi: 10.1371/journal.pone.0257965. eCollection 2021.

Abstract

Many important questions remain regarding severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the viral pathogen responsible for COVID-19. These questions include the mechanisms explaining the high percentage of asymptomatic but highly infectious individuals, the wide variability in disease susceptibility, and the mechanisms of long-lasting debilitating effects. Bioinformatic analysis of four coronavirus datasets representing previous outbreaks (SARS-CoV-1 and MERS-CoV), as well as SARS-CoV-2, revealed evidence of diverse host factors that appear to be coopted to facilitate virus-induced suppression of interferon-induced innate immunity, promotion of viral replication and subversion and/or evasion of antiviral immune surveillance. These host factors merit further study given their postulated roles in COVID-19-induced loss of smell and brain, heart, vascular, lung, liver, and gut dysfunction.

摘要

许多关于严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的重要问题仍然存在,SARS-CoV-2 是导致 COVID-19 的病毒病原体。这些问题包括解释高比例无症状但具有高度传染性个体的机制、疾病易感性的广泛变异性以及持久衰弱影响的机制。对代表先前爆发(SARS-CoV-1 和 MERS-CoV)以及 SARS-CoV-2 的四个冠状病毒数据集进行的生物信息学分析显示,存在多种宿主因素的证据,这些因素似乎被劫持以促进病毒诱导的干扰素诱导的先天免疫抑制、促进病毒复制以及颠覆和/或逃避抗病毒免疫监测。鉴于这些宿主因素在 COVID-19 引起的嗅觉丧失和脑、心脏、血管、肺、肝和肠道功能障碍中的假定作用,它们值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d6f/8480897/9688103cb4d3/pone.0257965.g001.jpg

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