Bramhadev Pattnaik1*, Pinaki Panigrahi2 and Mahendra P Yadav3
1One Health Center for Surveillance and Disease Dynamics, AIPH University,
Bhubaneswar, Odisha and Former Director, ICAR-Directorate of Foot and Mouth
Disease, Mukteshwar, India
2Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Georgetown University Medical Center, Washington, DC, USA
3Former Vice-Chancellor, SVP University of Agriculture and Technology, Meerut, India
*Corresponding Author: Bramhadev Pattnaik, One Health Center for Surveillance and Disease Dynamics, AIPH University, Bhubaneswar, Odisha and Former Director, ICAR-Directorate of Foot and Mouth Disease, Mukteshwar, India.
Received: May 22, 2020; Published: June 29, 2020
The novel coronavirus SARS-CoV-2 responsible for Coronavirus infectious disease of 2019 (COVID-19) in human, now a Global pandemic affecting 212 countries in all the five Continents, damages the cells that have ACE2 receptor expression on their surface. Hoffman., et al. (2020) observed that in addition to ACE2 receptor required for cellular attachment of the virion, cellular entry mechanism of the virus requires a cellular serine protease, TMPRSS2 and because alveolar type 2 cells express higher levels of both ACE2 and TMPRSS2 receptors, these cells might be the primary entry point for the virus in the lung. Intestine and kidney also have high expression of ACE2. The virus along with the ACE2 receptor enters the cells by endocytosis that results in reduction of ACE2 on cells, and as a consequence serum level of angiotensin II increases. Angiotensin II acts both as a vasoconstrictor and pro-inflammatory cytokine. Exposure to the virus does not necessarily cause infection, and not all people infected develop ARDS (acute respiratory distress syndrome) or succumb to the disease. Though people of all age group and sex are susceptible, the disease could be more fatal in elderly persons > 60 years of age. Extensive lung damage due to elicitation of Cytokine Storm (cytokine release syndrome; CRS) has been described by Hirano and Murakami (2020) and Shi., et al (2020). Role of specific HLA loci and alleles (class I or II) in developing protective immunity to this virus infection remains to be elucidated. It has been reported by Iwasaki and Yang (2020) that antibodies to SARS-CoV-2 at low concentrations as well as low affinity antibodies in the body can result in antibody-dependent enhancement (ADE) by utilizing Fc receptors on immune cells including macrophages, monocytes and B lymphocytes. ADE has detrimental effect in some patients with virus specific antibodies. High WBC count with associated lymphocytopenia is common in the COVID-19 patients. Ganji., et al. (2020) have reported significant reduction in the numbers of circulating lymphocytes and platelets, CD4+: CD8+ ratio of 2:1, and higher expression of CD8+ and hyperactivation of CTLs and no significant change in the expression level of CD4+ compared to healthy individuals. Anti-viral immune response to SARS-CoV-2 infection was due to over expression of CD8 and hyper activation of CTLs. Pathophysiology and pathology of the disease has been elaborated by Yuki., et al. (2020) and Sahu., et al (2020). The present review compiles the aspects of pathogenesis and involvement of the host immune system in aggravating the disease through the process of immune response.
Keywords: Coronavirus; COVID-19; Immunopathology; Immune Response; Pandemic; SARS
Citation: Bramhadev Pattnaik., et al. “Immunopathology of COVID-19 Caused by SARS-CoV-2: A Brief Review". Acta Scientific Microbiology 3.7 (2020): 79-88.
Copyright: © 2020 Bramhadev Pattnaik., 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.