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Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches

Authors Hasan A, Al-Ozairi E, Al-Baqsumi Z, Ahmad R, Al-Mulla F

Received 6 September 2020

Accepted for publication 22 December 2020

Published 9 March 2021 Volume 2021:10 Pages 63—85


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 6

Editor who approved publication: Professor Michael Shurin

Amal Hasan,1 Ebaa Al-Ozairi,2,3 Zahraa Al-Baqsumi,1 Rasheed Ahmad,1 Fahd Al-Mulla4

1Department of Immunology and Microbiology, Research Division, Dasman Diabetes Institute, Dasman, Kuwait City, Kuwait; 2Clinical Research Unit, Medical Division, Dasman Diabetes Institute, Dasman, Kuwait City, Kuwait; 3Department of Medicine, Faculty of Medicine, Jabriya, Kuwait City, Kuwait; 4Department of Genetics and Bioinformatics, Functional Genomics, Research Division, Dasman Diabetes Institute, Dasman, Kuwait City, Kuwait

Correspondence: Amal Hasan P.O. Box 1180, Dasman 15462, Kuwait
Tel +965 2224 2999 Ext. 4312
Email [email protected]

Abstract: Coronavirus disease 2019 (Covid-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can range in severity from asymptomatic to severe/critical disease. SARS-CoV-2 uses angiotensin-converting enzyme 2 to infect cells leading to a strong inflammatory response, which is most profound in patients who progress to severe Covid-19. Recent studies have begun to unravel some of the differences in the innate and adaptive immune response to SARS-CoV-2 in patients with different degrees of disease severity. These studies have attributed the severe form of Covid-19 to a dysfunctional innate immune response, such as a delayed and/or deficient type I interferon response, coupled with an exaggerated and/or a dysfunctional adaptive immunity. Differences in T-cell (including CD4+ T-cells, CD8+ T-cells, T follicular helper cells, γδ-T-cells, and regulatory T-cells) and B-cell (transitional cells, double-negative 2 cells, antibody-secreting cells) responses have been identified in patients with severe disease compared to mild cases. Moreover, differences in the kinetic/titer of neutralizing antibody responses have been described in severe disease, which may be confounded by antibody-dependent enhancement. Importantly, the presence of preexisting autoantibodies against type I interferon has been described as a major cause of severe/critical disease. Additionally, priorVaccine and multiple vaccine exposure, trained innate immunity, cross-reactive immunity, and serological immune imprinting may all contribute towards disease severity and outcome. Several therapeutic and preventative approaches have been under intense investigations; these include vaccines (three of which have passed Phase 3 clinical trials), therapeutic antibodies, and immunosuppressants.

Keywords: SARS-CoV-2, inflammation, immune regulation, neutralizing antibodies, cytokines, autoantibodies, type I interferon

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