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Severe Acute Respiratory Syndrome Coronavirus 2: From Gene Structure to Pathogenic Mechanisms and Potential Therapy.

ABSTRACT: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a newly emerging respiratory virus with high morbidity, which was named coronavirus disease 2019 (COVID-19) by World Health Organization (WHO). COVID-19 has triggered a series of threats to global public health. Even worse, new cases of COVID-19 infection are still increasing rapidly. Therefore, it is imperative that various effective vaccines and drugs should be developed to prevent and treat COVID-19 and reduce the serious impact on human beings. For this purpose, detailed information about the pathogenesis of COVID-19 at the cellular and molecular levels is urgently needed. In this review, we summarized the current understanding on gene structure, protein function, and pathogenic mechanisms of SARS-CoV-2. Based on the above, we refined the correlations among gene structure, protein function, and pathogenic mechanisms of SARS-CoV-2. Importantly, we further discussed potential therapeutic targets, aiming to accelerate the advanced design and development of vaccines and therapeutic drugs against COVID-19.

SUBMITTER: Wu J

PROVIDER: S-EPMC7347906 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Severe Acute Respiratory Syndrome Coronavirus 2: From Gene Structure to Pathogenic Mechanisms and Potential Therapy.

Wu Jun J Yuan Xiaohui X Wang Bing B Gu Rui R Li Wei W Xiang Xuemei X Tang Lijun L Sun Hongyu H

Frontiers in microbiology 20200703

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a newly emerging respiratory virus with high morbidity, which was named coronavirus disease 2019 (COVID-19) by World Health Organization (WHO). COVID-19 has triggered a series of threats to global public health. Even worse, new cases of COVID-19 infection are still increasing rapidly. Therefore, it is imperative that various effective vaccines and drugs should be developed to prevent and treat COVID-19 and reduce the serious impact ...[more]

PMID: 32719672

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Project description:UnlabelledSystems biology offers considerable promise in uncovering novel pathways by which viruses and other microbial pathogens interact with host signaling and expression networks to mediate disease severity. In this study, we have developed an unbiased modeling approach to identify new pathways and network connections mediating acute lung injury, using severe acute respiratory syndrome coronavirus (SARS-CoV) as a model pathogen. We utilized a time course of matched virologic, pathological, and transcriptomic data within a novel methodological framework that can detect pathway enrichment among key highly connected network genes. This unbiased approach produced a high-priority list of 4 genes in one pathway out of over 3,500 genes that were differentially expressed following SARS-CoV infection. With these data, we predicted that the urokinase and other wound repair pathways would regulate lethal versus sublethal disease following SARS-CoV infection in mice. We validated the importance of the urokinase pathway for SARS-CoV disease severity using genetically defined knockout mice, proteomic correlates of pathway activation, and pathological disease severity. The results of these studies demonstrate that a fine balance exists between host coagulation and fibrinolysin pathways regulating pathological disease outcomes, including diffuse alveolar damage and acute lung injury, following infection with highly pathogenic respiratory viruses, such as SARS-CoV.ImportanceSevere acute respiratory syndrome coronavirus (SARS-CoV) emerged in 2002 and 2003, and infected patients developed an atypical pneumonia, acute lung injury (ALI), and acute respiratory distress syndrome (ARDS) leading to pulmonary fibrosis and death. We identified sets of differentially expressed genes that contribute to ALI and ARDS using lethal and sublethal SARS-CoV infection models. Mathematical prioritization of our gene sets identified the urokinase and extracellular matrix remodeling pathways as the most enriched pathways. By infecting Serpine1-knockout mice, we showed that the urokinase pathway had a significant effect on both lung pathology and overall SARS-CoV pathogenesis. These results demonstrate the effective use of unbiased modeling techniques for identification of high-priority host targets that regulate disease outcomes. Similar transcriptional signatures were noted in 1918 and 2009 H1N1 influenza virus-infected mice, suggesting a common, potentially treatable mechanism in development of virus-induced ALI.

Dataset Information

Severe Acute Respiratory Syndrome Coronavirus 2: From Gene Structure to Pathogenic Mechanisms and Potential Therapy.

Publications

Severe Acute Respiratory Syndrome Coronavirus 2: From Gene Structure to Pathogenic Mechanisms and Potential Therapy.

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