Severe COVID-19: what have we learned with the immunopathogenesis?
Abstract The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS- CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.
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Sociedade Brasileira de Reumatologia
2020
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oai:scielo:S2523-310620200001004012020-10-02Severe COVID-19: what have we learned with the immunopathogenesis?Bordallo,BrunoBellas,MozartCortez,Arthur FernandesVieira,MatheusPinheiro,Marcelo COVID-19 SARS-CoV-2 Immunology Inflammation Cytokine storm Cytokine Macrophage activation syndrome Thrombosis Abstract The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS- CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.info:eu-repo/semantics/openAccessSociedade Brasileira de ReumatologiaAdvances in Rheumatology v.60 20202020-01-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S2523-31062020000100401en10.1186/s42358-020-00151-7 |
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Bordallo,Bruno Bellas,Mozart Cortez,Arthur Fernandes Vieira,Matheus Pinheiro,Marcelo |
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Bordallo,Bruno Bellas,Mozart Cortez,Arthur Fernandes Vieira,Matheus Pinheiro,Marcelo Severe COVID-19: what have we learned with the immunopathogenesis? |
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Bordallo,Bruno Bellas,Mozart Cortez,Arthur Fernandes Vieira,Matheus Pinheiro,Marcelo |
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Bordallo,Bruno |
title |
Severe COVID-19: what have we learned with the immunopathogenesis? |
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Severe COVID-19: what have we learned with the immunopathogenesis? |
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Severe COVID-19: what have we learned with the immunopathogenesis? |
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Severe COVID-19: what have we learned with the immunopathogenesis? |
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Severe COVID-19: what have we learned with the immunopathogenesis? |
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severe covid-19: what have we learned with the immunopathogenesis? |
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Abstract The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself. Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena. Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS- CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19. |
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Sociedade Brasileira de Reumatologia |
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2020 |
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http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2523-31062020000100401 |
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