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Severe COVID-19: what have we learned with the immunopathogenesis?
Adv Rheumatol. 2020 09 22; 60(1):50.AR

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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Authors+Show Affiliations

Bordallo B
Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Univesidade Federal Fluminense, Niterói, RJ, Brazil. brunobaf@hotmail.com.
Bellas M
Departament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Universidade Federal Fluminense, Niterói, RJ, Brazil.
Cortez AF
Hospital Universitário Gaffré e Guinle / Universidade Federal do Estado do Rio de Janeiro, Internal Medicine Departament, Rio de Janeiro, RJ, Brazil.
Vieira M
Departament of Internal Medicine, Hospital Universitário Clementino Fraga Filho, Rio de Janeiro, RJ, Brazil.
Pinheiro M
Departament of Rheumatology, Universidade Federal de São Paulo, Sao Paulo, SP, Brazil.

MeSH

Age FactorsAngiotensin-Converting Enzyme 2AnimalsAntibody FormationBetacoronavirusBlood Coagulation DisordersCOVID-19ComorbidityCoronavirus InfectionsCytokine Release SyndromeHumansImmunity, InnateInflammationLungLymphopeniaMiceMiddle East Respiratory Syndrome CoronavirusPandemicsPeptidyl-Dipeptidase APneumonia, ViralRespiratory Distress SyndromeRisk FactorsSARS-CoV-2Severe Acute Respiratory SyndromeSeverity of Illness IndexSex FactorsVirus Internalization

Pub Type(s)

Journal Article
Systematic Review

Language

eng

PubMed ID

32962761

Citation

Bordallo, Bruno, et al. "Severe COVID-19: what Have We Learned With the Immunopathogenesis?" Advances in Rheumatology (London, England), vol. 60, no. 1, 2020, p. 50.
Bordallo B, Bellas M, Cortez AF, et al. Severe COVID-19: what have we learned with the immunopathogenesis? Adv Rheumatol. 2020;60(1):50.
Bordallo, B., Bellas, M., Cortez, A. F., Vieira, M., & Pinheiro, M. (2020). Severe COVID-19: what have we learned with the immunopathogenesis? Advances in Rheumatology (London, England), 60(1), 50. https://doi.org/10.1186/s42358-020-00151-7
Bordallo B, et al. Severe COVID-19: what Have We Learned With the Immunopathogenesis. Adv Rheumatol. 2020 09 22;60(1):50. PubMed PMID: 32962761.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Severe COVID-19: what have we learned with the immunopathogenesis? AU - Bordallo,Bruno, AU - Bellas,Mozart, AU - Cortez,Arthur Fernandes, AU - Vieira,Matheus, AU - Pinheiro,Marcelo, Y1 - 2020/09/22/ PY - 2020/06/18/received PY - 2020/09/07/accepted PY - 2020/9/23/entrez PY - 2020/9/24/pubmed PY - 2020/10/8/medline KW - COVID-19 KW - Cytokine KW - Cytokine storm KW - Immunology KW - Inflammation KW - Macrophage activation syndrome KW - SARS-CoV-2 KW - Thrombosis SP - 50 EP - 50 JF - Advances in rheumatology (London, England) JO - Adv Rheumatol VL - 60 IS - 1 N2 - 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. SN - 2523-3106 UR - https://www.unboundmedicine.com/medline/citation/32962761/Severe_COVID_19:_what_have_we_learned_with_the_immunopathogenesis DB - PRIME DP - Unbound Medicine ER -