EREN ŞAHİN, ALİ DAĞ, FATİH EREN
Turkish Medical Student Journal - 2023;10(2):91-96
An agent that emerged with a series of pneumonia cases of unknown etiology in China in December 2019 and caused the coronavirus disease-2019 pandemic, has been defined as severe acute respiratory syndrome coronavirus 2 as a result of studies conducted in a group of patients presenting with cough, dyspnea, and pyrexia. Viral entry into host cells starts and affects critical steps of pathogenesis. This step includes host receptor-viral spike protein interaction and enzyme activity. Varying degrees of host responses to viral entry are observed among individuals. Polymorphisms, that may be detected in communities and attributed to host cells, have a role in the pathogenesis of coronavirus disease infection. The reason why this has been considered is that receptors, enzymes, and other physiological response mechanisms’ structures are idiosyncratic. Genetic variants that aid spike 1 protein and angiotensin-converting enzyme 2 binding are associated with susceptibility to infection because it is easier for the viruses to enter cells. On the contrary, genetic variants that inhibit binding are related to better outcomes because it is harder for the virus to invade. The transmembrane protease serine gene is another region for genetic polymorphisms. When there is a genetic variant in the regulatory region two outcomes can occur: up-regulation or down-regulation. Since the transmembrane protease serine gene oversees viral entry, up-regulation or high expression of this gene causes worse outcomes. Specifically, the rs2285666 variant of the angiotensin-converting enzyme 2 gene is found to decrease expression, making it protective, while the rs12329760 variant of the transmembrane serine protease gene makes patients more susceptible to worse consequences. Many other variants of genes are associated with coronavirus disease, but they require further careful investigation to understand the mechanism behind the relation. Human leukocyte antigen and AB0 blood group genes, vitamin metabolism genes, and others are found to have a role in coronavirus disease pathophysiology. This study aims to show most of the probable polymorphic sites of host cell genetics that may influence the pathogenesis of coronavirus disease.
