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Molecular mechanisms and pharmacological interventions in the replication cycle of human coronaviruses
Genetics and Molecular Biology ( IF 1.7 ) Pub Date : 2021-01-01 , DOI: 10.1590/1678-4685-gmb-2020-0212
Fernando Moreira Simabuco 1 , Rodrigo Esaki Tamura 2 , Isadora Carolina Betim Pavan 3 , Mirian Galliote Morale 4 , Armando Morais Ventura 4
Affiliation  

Abstract SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2), as well as SARS-CoV from 2003 along with MERS-CoV from 2012, is a member of the Betacoronavirus genus of the Nidovirales order and is currently the cause of the pandemic called COVID-19 (or Coronavirus disease 2019). COVID-19, which is characterized by cough, fever, fatigue, and severe cases of pneumonia, has affected more than 23 million people worldwide until August 25th, 2020. Here, we present a review of the cellular mechanisms associated with human coronavirus replication, including the unique molecular events related to the replication transcription complex (RTC) of coronaviruses. We also present information regarding the interactions between each viral protein and cellular proteins associated to known host-pathogen implications for the coronavirus biology. Finally, a specific topic addresses the current attempts for pharmacological interventions against COVID-19, highlighting the possible effects of each drug on the molecular events of viral replication. This review intends to aid future studies for a better understanding of the SARS-CoV-2 replication cycle and the development of pharmacological approaches targeting COVID-19.

中文翻译:

人类冠状病毒复制周期的分子机制和药理干预

摘要 SARS-CoV-2(严重急性呼吸系统综合症冠状病毒 2)以及 2003 年的 SARS-CoV 和 2012 年的 MERS-CoV,是 Nidovirales 目 Betacoronavirus 属的成员,目前是大流行的原因称为 COVID-19(或 2019 年冠状病毒病)。到 2020 年 8 月 25 日,以咳嗽、发烧、疲劳和严重肺炎为特征的 COVID-19 已影响全球超过 2300 万人。在此,我们回顾了与人类冠状病毒复制相关的细胞机制,包括与冠状病毒复制转录复合物 (RTC) 相关的独特分子事件。我们还提供了有关每种病毒蛋白与与已知宿主病原体对冠状病毒生物学的影响相关的细胞蛋白之间相互作用的信息。最后,一个特定主题涉及当前针对 COVID-19 的药物干预尝试,强调每种药物对病毒复制分子事件的可能影响。本综述旨在帮助未来的研究更好地了解 SARS-CoV-2 复制周期和针对 COVID-19 的药理学方法的开发。
更新日期:2021-01-01
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