Clinical Manifestations of Cytokine Storm and Immune Response to COVID-19: Literature Review

Abstract

Spreading COVID-19 disease caused by coronavirus 2 causes tremendous health challenges worldwide. Owing to a high transmission rate, fast-spreading disease, asymptomatic carriers, and high infectivity, we observe a pandemic status that we follow today. Although there are different reports of case fatality rates around the globe, the primary determinant of mortality is age. Symptoms of COVID-19 disease vary from asymptomatic individuals to severe acute respiratory distress syndrome (ARDS) and death. The most common complication of COVID-19 is ARDS. Hyperinflammation due to excessive immune response to coronavirus is the leading cause of severe symptoms seen in the course of COVID-19. The virus enters cells utilizing the S1 subunit through the ACE2 receptor. The innate immune response is the primary immune reaction to virus entry. RNA viruses, including coronavirus, replicate in the cytoplasm, assemble, and then exit by exocytosis. Some suggest that SARS-Cov2 uses cell-cell fusion to infect adjacent cells. Different sensors detect the virus particles in the endosomal compartment and cytoplasm, and infected cells induce an immune response to surrounding cells. As a result, the production of cytokines and chemokines such as interferons (INFs) will be augmented. Since coronavirus uses different means to evade the immune system, it is difficult for immune cells to "sense" them; thus, the coronavirus response is not adequate. It has been showing that even a sufficient level of immunoglobulin response couldn't neutralize virus replication. Therefore, the innate immune response is unable to eradicate SARS-Cov2, causes overexpression of cytokines and chemokines that cannot eliminate the virus. Diminished INFs secretion and apoptosis of regulatory T cells (Treg) are the leading cause of dysregulated immune response in a cytokine storm. Inflammatory cells attack infected and uninfected cells, causing more inflammation How to cite this paper: