Gene Associated Divergence of COVID-19 Morbidity & COVID-19 Vaccines

Abstract

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), also known as COVID-19, drastically changed our everyday lives. It has indeed caused a considerable increase in morbidity and mortality rates worldwide. There is an underlying complex interplay between the infectious agents and the human host, which is related to different biological mechanisms. Phenotypic spectrums associated with SARS-CoV-2 infection or COVID-19 range from asymptomatic to severe systemic complications such as pneumonia, respiratory failure, and death. Around 15 % of cases are severe. Some are accompanied by a dysregulated immune system or a cytokine storm, and others with both. There is increasing evidence that the severe manifestations of COVID-19 might attribute to human genetic variants. Polymorphisms in genes that are related to immune deficiency and or inflammasome activation (cytokine storm) are examples of these variants. The question is, is the variability of the hosts’ genetic background the reason behind the different responses to COVID-19? Or are there other factors? Case reports and GWAS studies showed that the susceptibility to severe viral infections was associated with the genetic variants in the immune response genes. Identifying the candidate’s genes is likely to aid in explaining why COVID-19 symptoms are severe to some but not others. Not to mention that it will provide insights that help us further understand the pathogenesis of severe COVID-19, to then make it possible to come out with more effective treatments and vaccines. Global DNA methylation, ACE2 gene methylation and post-translational histone modifications drive differences in host tissue-, biological age- and sex-biased patterns of viral infection. Epigenetic changes impact genome stabilization, maintenance of cellular homeostasis, and affect the pathophysiology of the viral infection