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The Immune Response and Immunopathology of COVID-19.
Front Immunol. 2020; 11:2037.FI

Abstract

Coronaviruses were first discovered in the 1960s and are named due to their crown-like shape. Sometimes, but not often, a coronavirus can infect both animals and humans. An acute respiratory disease, caused by a novel coronavirus (severe acute respiratory syndrome coronavirus-2 or SARS-CoV-2 previously known as 2019-nCoV) was identified as the cause of coronavirus disease 2019 (COVID-19) as it spread throughout China and subsequently across the globe. As of 14th July 2020, a total of 13.1 million confirmed cases globally and 572,426 deaths had been reported by the World Health Organization (WHO). SARS-CoV-2 belongs to the β-coronavirus family and shares extensive genomic identity with bat coronavirus suggesting that bats are the natural host. SARS-CoV-2 uses the same receptor, angiotensin-converting enzyme 2 (ACE2), as that for SARS-CoV, the coronavirus associated with the SARS outbreak in 2003. It mainly spreads through the respiratory tract with lymphopenia and cytokine storms occuring in the blood of subjects with severe disease. This suggests the existence of immunological dysregulation as an accompanying event during severe illness caused by this virus. The early recognition of this immunological phenotype could assist prompt recognition of patients who will progress to severe disease. Here we review the data of the immune response during COVID-19 infection. The current review summarizes our understanding of how immune dysregulation and altered cytokine networks contribute to the pathophysiology of COVID-19 patients.

Authors+Show Affiliations

Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Mycobacteriology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Masih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Division of Pharmacology, Faculty of Science, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, Netherlands.Respiratory Section, Faculty of Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom. Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

32983152

Citation

Mortaz, Esmaeil, et al. "The Immune Response and Immunopathology of COVID-19." Frontiers in Immunology, vol. 11, 2020, p. 2037.
Mortaz E, Tabarsi P, Varahram M, et al. The Immune Response and Immunopathology of COVID-19. Front Immunol. 2020;11:2037.
Mortaz, E., Tabarsi, P., Varahram, M., Folkerts, G., & Adcock, I. M. (2020). The Immune Response and Immunopathology of COVID-19. Frontiers in Immunology, 11, 2037. https://doi.org/10.3389/fimmu.2020.02037
Mortaz E, et al. The Immune Response and Immunopathology of COVID-19. Front Immunol. 2020;11:2037. PubMed PMID: 32983152.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Immune Response and Immunopathology of COVID-19. AU - Mortaz,Esmaeil, AU - Tabarsi,Payam, AU - Varahram,Mohammad, AU - Folkerts,Gert, AU - Adcock,Ian M, Y1 - 2020/08/26/ PY - 2020/05/02/received PY - 2020/07/27/accepted PY - 2020/9/28/entrez PY - 2020/9/29/pubmed PY - 2020/10/21/medline KW - IL-6 KW - SARS-CoV KW - SARS-CoV-2 KW - coronavirus KW - cytokines storm KW - pathogenesis SP - 2037 EP - 2037 JF - Frontiers in immunology JO - Front Immunol VL - 11 N2 - Coronaviruses were first discovered in the 1960s and are named due to their crown-like shape. Sometimes, but not often, a coronavirus can infect both animals and humans. An acute respiratory disease, caused by a novel coronavirus (severe acute respiratory syndrome coronavirus-2 or SARS-CoV-2 previously known as 2019-nCoV) was identified as the cause of coronavirus disease 2019 (COVID-19) as it spread throughout China and subsequently across the globe. As of 14th July 2020, a total of 13.1 million confirmed cases globally and 572,426 deaths had been reported by the World Health Organization (WHO). SARS-CoV-2 belongs to the β-coronavirus family and shares extensive genomic identity with bat coronavirus suggesting that bats are the natural host. SARS-CoV-2 uses the same receptor, angiotensin-converting enzyme 2 (ACE2), as that for SARS-CoV, the coronavirus associated with the SARS outbreak in 2003. It mainly spreads through the respiratory tract with lymphopenia and cytokine storms occuring in the blood of subjects with severe disease. This suggests the existence of immunological dysregulation as an accompanying event during severe illness caused by this virus. The early recognition of this immunological phenotype could assist prompt recognition of patients who will progress to severe disease. Here we review the data of the immune response during COVID-19 infection. The current review summarizes our understanding of how immune dysregulation and altered cytokine networks contribute to the pathophysiology of COVID-19 patients. SN - 1664-3224 UR - https://www.unboundmedicine.com/medline/citation/32983152/The_Immune_Response_and_Immunopathology_of_COVID_19_ L2 - https://doi.org/10.3389/fimmu.2020.02037 DB - PRIME DP - Unbound Medicine ER -