ABSTRACT
Angiotensin-converting enzyme (ACE) and its homologue, ACE2, have been mostly associated with hypertensive disorder. However, recent pandemia of SARS-CoV-2 has put these proteins at the center of attention, as this virus has been shown to exploit ACE2 protein to enter cells. Clear difference in the response of affected patients to this virus has urged researchers to find the molecular basis and pathophysiology of the cell response to this virus. Different levels of expression and function of ACE proteins, underlying disorders, consumption of certain medications and the existence of certain genomic variants within ACE genes are possible explanations for the observed difference in the response of individuals to the SARS-CoV-2 infection. In the current review, we discuss the putative mechanisms for this observation.
ABSTRACT
The recent outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global crisis, necessitating the identification of genetic factors that modulate the risk of disorder or its severity. The current data about the role of genetic risk factors in determination of rate of SARS-CoV-2 infection in each ethnic group and the severity of disorder is limited. Moreover, several confounding parameters such as the number of tests performed in each country, the structure of the population especially the age distribution, the presence of risk factors for respiratory disorders such as smoking and other environmental factors might be involved in the variability in disease course or prevalence of infection among different ethnic groups. However, assessment of the role of genetic variants in determination of the course of other respiratory infections might help in recognition of possible candidate for further analysis in patients affected with SARS-CoV-2. In the current review, we summarize the data showing the association between genomic variants and risk of acute respiratory distress syndrome, respiratory infections or severity of these conditions with an especial focus on the SARS-CoV-2.
Subject(s)
Coronavirus Infections , Pandemics , Pneumonia, Viral , Respiratory Tract Infections/genetics , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/genetics , Coronavirus Infections/physiopathology , Genetic Predisposition to Disease , Genetic Variation , Humans , Pneumonia, Viral/epidemiology , Pneumonia, Viral/genetics , Pneumonia, Viral/physiopathology , Polymorphism, Single Nucleotide , Respiratory Tract Infections/physiopathology , SARS-CoV-2 , Severity of Illness IndexABSTRACT
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global pandemic in early 2020. The infection has been associated with a wide range of clinical symptoms. In the severely affected patients, it has caused dysregulation of immune responses including over-secretion of inflammatory cytokines and imbalances in the proportion of naïve helper T cells, memory helper T cells and regulatory T cells. Identification of the underlying mechanism of such aberrant function of immune system would help in the prediction of disease course and selection of susceptible patients for more intensive cares. In the current review, we summarize the results of studies which reported alterations in cytokine levels and immune cell functions in patients affected with SARS-CoV-2 and related viruses.