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1.
Adv Rheumatol ; 60:50-50, 2020.
Article in English | LILACS (Americas) | ID: grc-742198

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.

2.
Adv Rheumatol ; 60(1): 50, 2020 09 22.
Article in English | MEDLINE | ID: covidwho-781570

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.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Pneumonia, Viral/immunology , Respiratory Distress Syndrome/immunology , Age Factors , Angiotensin-Converting Enzyme 2 , Animals , Antibody Formation , Betacoronavirus/pathogenicity , Blood Coagulation Disorders/etiology , COVID-19 , Comorbidity , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Humans , Immunity, Innate , Inflammation/immunology , Lung/pathology , Lymphopenia/immunology , Mice , Middle East Respiratory Syndrome Coronavirus/immunology , Pandemics , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Risk Factors , SARS-CoV-2 , Severe Acute Respiratory Syndrome/immunology , Severity of Illness Index , Sex Factors , Virus Internalization
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