Editorial
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Dec 6, 2020; 8(23): 5835-5843
Published online Dec 6, 2020. doi: 10.12998/wjcc.v8.i23.5835
Understanding the immunopathogenesis of COVID-19: Its implication for therapeutic strategy
Yukihiro Shimizu
Yukihiro Shimizu, Gastroenterology Center, Nanto Municipal Hospital, Nanto 932-0211, Toyama, Japan
Author contributions: Yukihiro Shimizu alone designed and wrote the paper.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yukihiro Shimizu, MD, PhD, Director, Doctor, Gastroenterology Center, Nanto Municipal Hospital, 938 Inami, Nanto 932-0211, Toyama, Japan. rsf14240@nifty.com
Received: May 15, 2020
Peer-review started: May 15, 2020
First decision: November 3, 2020
Revised: November 12, 2020
Accepted: November 21, 2020
Article in press: November 21, 2020
Published online: December 6, 2020
Processing time: 203 Days and 1.2 Hours
Abstract

Although 80% of individuals infected with the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) recover without antiviral treatments, the other 20% progress to severe forms of pulmonary disease, suggesting that the host’s immune response to the virus could influence the outcome of coronavirus disease 2019 (COVID-19). SARS-CoV-2 infects alveolar epithelial type 2 cells expressing angiotensin-converting enzyme 2, and these infected epithelial cells recruit dendritic cells, neutrophils and monocytes /macrophages, leading to the activation of CD4+ and CD8+ T cells. These cells launch an antiviral immune response, but are able to completely suppress viral replication or completely eradicate virus in a limited proportion of infected patients. In other patients, viral suppression is incomplete and the numbers of circulating B and T cells are subsequently reduced by as yet unknown mechanisms. Some patients with sustained viral replication progress to a severe condition called cytokine storm. Although antiviral drug(s) should be considered early in infection to prevent progression, there have been no antiviral therapies proven to be effective for significantly inhibiting the viral replication in vivo and suppressing the progression to cytokine storm. Blocking the action of cytokines with dexamethasone or anti-interleukin-6 could have a pivotal role in treatment of those patients. Therapeutic strategy should therefore be based on viral kinetics and the immunopathology of COVID-19.

Keywords: COVID-19; SARS-CoV-2; Immune response; Antibody; Viral kinetics; Treatment

Core Tip: Since the coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), the core therapeutic strategy should be aimed at the eradication of the virus. Unfortunately, there have been no antiviral drugs proven to be effective for this viral infection. The pathogenesis of SARS-CoV-2 is formed by the interaction between the viral infection and the immune response to the virus, and the various clinical features observed in patients with COVID-19 could be due to differences in host immune responses. Moreover, therapeutic strategies should be based on both viral kinetics and the immune response. This editorial summarizes current understanding about immune responses in patients infected with SARS-CoV-2 and provides clues to therapeutic strategies based on this information.