COVID-19 and cytokine storm Mukherjee Kakali* Department of Biotechnology, Heritage Institute of Technology, Kolkata, West Bengal, India *Corresponding author: Kakali Mukherjee, Department of Biotechnology, Heritage Institute of Technology, Kolkata, West Bengal, India, E-mail: kakali.mukherjee@heritageit.edu
Online published on 24 May, 2021. Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is the pathogen that causes coronavirus disease 2019 (COVID-19). As of October 31, 2020, the outbreak of COVID-19 has caused 1,201,902 deaths around the world including 122,000 in India. The current evidence showed that severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who are moderately ill. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 cells, has been found in lung tissues of patients with COVID-19 by postmortem examination. Recently, increasing studies indicate that the “cytokine storm” may contribute to the mortality of COVID-19. This review focuses on the cytokine storm (CS) in the context of infection, with particular emphasis on respiratory viruses and shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. It is also highlighted how high-throughput genomic methods are revealing new insights into the CS. Finally, how current evidence indicates that Tocilizumab, an IL-6 inhibitor, is relatively effective and safe, besides corticosteroids, programmed cell death protein (PD)-1/PD-L1 checkpoint inhibition, cytokine-adsorption devices, intravenous immunoglobulin, and antimalarial agents could be potentially useful are also discussed. Top Keywords Acute respiratory distress syndrome, COVID-19, Cytokine storm mediators, Cytokine storm, Cytokine, Gene expression kinetics, Immunoregulation, Interleukin-6, Treatment strategies. Top |