ABSTRACT
Some risk causes may be associated with the severity of COVID-19. The central host-pathogen factors might affect infection are human receptor angiotensin-converting enzyme 2 (ACE2), trans-membrane protease serine 2 (TMPRSS2), and SARS-CoV-2 surface spike (S)-protein. The main purpose of this study was to determine the differences in the expression the metalloproteinases-2 (MMP-2), MMP-9, ACE2, and TMPRSS2 genes and their correlation with lymphopenia in the mild and severe types of the COVID-19 patients. Eighty-eight patients, aged 36 to 60 years old with the mild (n=44) and severe (n=44) types of COVID-19 were enrolled. Total RNA was isolated from the peripheral blood mononuclear cells (PBMCs). The changes of MMP-2, MMP-9, ACE2 and TMPRSS2 gene expression in PBMCs from mild and severe COVID-19 patients were examined by the real time-quantitative polymerase chain reaction (RT-qPCR) assay and, compared between the groups. Data were collected from May 2021 to March 2022. The mean age of the patients in both groups was 48 (interquartile range, 36-60), and there were no appreciable differences in age or gender distribution between the two groups. The present study showed that a significant increase in the expression of ACE2, TMPRSS2, MMP-2, and MMP-9 genes in the severe type of the COVID-19 patients compared, to the mild type of the COVID-19 patients. Overall, it suggests the expression levels of these genes on the PBMC surface in the immune system are susceptible to infection by SARS-COV-2 and therefore could potentially predict the patients' outcome.
Subject(s)
COVID-19 , Lymphopenia , Humans , Adult , Middle Aged , COVID-19/genetics , SARS-CoV-2 , Angiotensin-Converting Enzyme 2/genetics , Leukocytes, Mononuclear , Matrix Metalloproteinase 2/genetics , Matrix Metalloproteinase 9/genetics , Lymphopenia/genetics , Serine Endopeptidases/geneticsABSTRACT
In 2020, a deadly pandemic caused by the SARS-COV-2 virus spread worldwide and killed many people. In some viral infections, in addition to the pathogenic role of the virus, impaired immune function leads to inflammation and further damage in internal tissues. For example, coronavirus in some patients prevents the stimulation of the acquired immune system. Therefore, innate immunity is over-stimulated to compensate, followed by the overproduction of inflammatory cytokines and cytokine storm. Various underlying factors such as age, gender, blood pressure, diabetes, and obesity affect cytokine storm. It seems that cytokine storm is one of the leading causes of death among COVID-19 patients, and providing that this storm is detected and controlled in time, it can reduce the mortality of COVID-19 patients. This article aims to investigate the immune system response to COVID-19, various factors associated with cytokine storm, and its treatment. In the current situation, in parallel with the progress made in the field of vaccination, it is necessary to carefully examine the various dimensions of the immune system in response to the COVID-19 virus to seek a suitable treatment strategy to save the lives of patients in intensive care units [ FROM AUTHOR] Copyright of European Journal of Inflammation is the property of Sage Publications Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
ABSTRACT
No Abstract.