Volume 2, Issue 1 (2021)
- *Corresponding Author:
- Dr. Yulia Khodneva
Division of Cardiovascular Disease, Department of Medicine, School of Medicine, University of Alabama at Birmingham, 1717 11th Avenue South, MT 509, Birmingham AL 35294, USA.
Tel: +1 (205) 934-2884
Received date: Jun 02, 2021; Accepted date: June 15, 2021; Published date: June 22, 2021
Citation: Fu RH, Xie M, Oparil S, Khodneva Y. Immune Responses to SARS-CoV-2. J Clin Microbiol Immunol. 2021;2(1):14-19.
Copyright: © 2021 Fu RH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Since the onset of the COVID-19 pandemic, there have been over 100 million cases of the disease worldwide. Although the overall mortality rate of COVID-19 remains relatively low at approximately 2%, the highest mortality rate has been observed in patients with severe cases of COVID-19, reaching as high as 77%. Although researchers and clinicians continue developing treatments for severe COVID-19, the mechanisms that regulate the development of severe disease are complex and relatively unknown. The objective of this review is to summarize the differences between mild and severe cases of COVID-19 and their distinct effects on the immune system and its cells/proteins, including differences in the innate and adaptive immune responses triggered by varying degrees of disease severity. Identification of the mechanisms responsible for the development of severe COVID-19 may offer potential targets for future prevention and treatment methods that can reduce mortality rates from severe COVID-19. This review focuses on cytokine storm formation as the primary mechanism for severe COVID-19 development and explores alternative mechanisms that have been identified, such as how COVID-19-induced interferon loss inhibits the body’s viral suppression capabilities and how different blood types may play a role in facilitating viral infection or protecting against it.
Severe COVID-19; SARS-CoV-2; Immune system; Cytokine storm.