The Role of Cytokines and Chemokines in Severe Acute Respiratory Syndrome Coronavirus 2 Infections
Journal
Frontiers in Immunology
Journal Volume
13
Date Issued
2022
Author(s)
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in countless infections and caused millions of deaths since its emergence in 2019. Coronavirus disease 2019 (COVID-19)-associated mortality is caused by uncontrolled inflammation, aberrant immune response, cytokine storm, and an imbalanced hyperactive immune system. The cytokine storm further results in multiple organ failure and lung immunopathology. Therefore, any potential treatments should focus on the direct elimination of viral particles, prevention strategies, and mitigation of the imbalanced (hyperactive) immune system. This review focuses on cytokine secretions of innate and adaptive immune responses against COVID-19, including interleukins, interferons, tumor necrosis factor-alpha, and other chemokines. In addition to the review focus, we discuss potential immunotherapeutic approaches based on relevant pathophysiological features, the systemic immune response against SARS-CoV-2, and data from recent clinical trials and experiments on the COVID-19-associated cytokine storm. Prompt use of these cytokines as diagnostic markers and aggressive prevention and management of the cytokine storm can help determine COVID-19-associated morbidity and mortality. The prophylaxis and rapid management of the cytokine storm appear to significantly improve disease outcomes. For these reasons, this study aims to provide advanced information to facilitate innovative strategies to survive in the COVID-19 pandemic. Copyright © 2022 Hsu, Yu, Peng, Ye, Hu, Chong, Yap, Lee, Lin and Yu.
Subjects
chemokines; COVID-19; cytokines; diagnostic markers; infection
SDGs
Other Subjects
atazanavir; C reactive protein; CD14 antigen; chemokine; cytokine; eculizumab; escitalopram; ferritin; fractalkine; gamma interferon; gamma interferon inducible protein 10; granulocyte macrophage colony stimulating factor; high mobility group B1 protein; hydroxychloroquine; intercellular adhesion molecule 1; interferon; interleukin 1; interleukin 10; interleukin 13; interleukin 15; interleukin 17; interleukin 18; interleukin 1beta; interleukin 2; interleukin 22; interleukin 4; interleukin 6; interleukin 7; interleukin 8; Janus kinase 2; lopinavir; monocyte chemotactic protein 1; myeloperoxidase; programmed death 1 ligand 1; RANTES; remdesivir; sarilumab; siltuximab; tocilizumab; toll like receptor 2; tumor necrosis factor; chemokine; cytokine; acute kidney failure; anorexia; arthralgia; artificial ventilation; ataxia; atherosclerosis; bronchoalveolar lavage fluid; bronchoconstriction; CD8+ T lymphocyte; cell proliferation; cerebellar ataxia; choroid plexus; chronic kidney failure; cognitive defect; complement activation; coronavirus disease 2019; cytokine production; cytokine storm; cytotoxicity; demyelination; dengue; disease severity; dyslipidemia; endothelium cell; hospitalization; human; humoral immunity; hyperglycemia; hypertension; hypotension; hypoxia; immune response; immune system; immunopathology; lung embolism; lung ventilation; microglia; Middle East respiratory syndrome coronavirus; morbidity; mortality; multiple organ failure; myofibroblast; neutrophil; oxygen saturation; pediatric multisystem inflammatory syndrome; pneumonia; prophylaxis; protein expression; pyroptosis; regulatory T lymphocyte; renin angiotensin aldosterone system; Review; Severe acute respiratory syndrome coronavirus 2; systematic review; Th1 cell; Th17 cell; Zika fever; cytokine release syndrome; pandemic; Chemokines; COVID-19; Cytokine Release Syndrome; Cytokines; Humans; Pandemics; SARS-CoV-2
Type
review