Severe COVID-19: what have we learned with the immunopathogenesis?
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(2020) 60:50
Advances in Rheumatology
REVIEW
Open Access
Severe COVID-19: what have we learned with the immunopathogenesis? Bruno Bordallo1* , Mozart Bellas2, Arthur Fernandes Cortez3, Matheus Vieira4 and Marcelo Pinheiro5
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 SARSCoV-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. Keywords: COVID-19, SARS-CoV-2, Immunology, Inflammation, Cytokine storm, Cytokine, Macrophage activation syndrome, Thrombosis
Background The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNAenveloped virus, is the causative agent of coronavirus disease 2019 (COVID-19), being first identified in Wuhan, China, in December 2019. Previously, other epidemic coronavirus such as severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002 and the middle-east respiratory syndrome coronavirus (MERSCoV) in 2012, had serious impact on human health and warned the world about the possible reemergence of new pathogenic strains [1]. Despite being a new virus, several common morpho-functional characteristics have been reported between SARS-CoV and the SARS-CoV2, including the interaction of the viral spike (S) glycoprotein with the human angiotensin converting enzyme * Correspondence: [email protected] 1 Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Univesidade Federal Fluminense, Niterói, RJ, Brazil Full list of author information is available at the end of the article
2 (ACE2). These similarities may help understanding some pathophysiological mechanisms and pointing out possible therapeutic targets. The first step for SARS-CoV-2 entry into the host cell is the interaction between the S glycoprotein and ACE2 on cell surface. Since the latter acts as a viral receptor, the virus will only infect ACE2 expressing cells, notably type II pneumocytes. These cells represent 83% of the ACE2-expressing cells in humans, but cells from other tissues and organs, such as heart, kidney, intestine and endothelium, can also express this receptor [2].
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