COVID-19: pathogenesis, genetic polymorphism, clinical features and laboratory findings

Abstract

COVID-19 caused by a novel agent SARS-CoV-2 progressed to a pandemic condition and resulted in a major public health concern worldwide, leading to social and economic issues at the same time. The pathogenesis of COVID-19 starts with the bonding of the virus to ACE2 receptors expressed in many tissues, and the triggered excessive immune response plays a critical role in the course of the disease. The cytokine storm that occurs upon excessive production of pro-inflammatory cytokines is considered responsible for the severe progression of the disease and the organ damage. However, the accurate pathophysiological mechanism of the disease, which progresses with various clinical presentations, is still substantially unknown. While various studies have been conducted on the effect of genetic polymorphism on the course and severity of the disease, the presence of a significant effect has not been proven yet. The clinical course of the disease is variable, with clinical representation ranging from 81% mild course to 14% severe course along with 5% critical course in patients. Asymptomatic course is considered to be higher than expected, although its frequency is not known exactly. Older adults and those with comorbidities are exposed to a more severe disease course. The disease progress with various symptoms, such as fever, cough, dyspnea, malaise, myalgia, taste and smell dysfunctions, diarrhea, and headache. A range of complications (acute respiratory distress syndrome, thromboembolic conditions, arrhythmia and cardiac events, secondary infections) could be seen during the course of the disease. Varied laboratory tests are vital to determine these verity and prognosis of the disease, along with the condition and exposure of the affected systems during thecourse of COVID-19.

Impact of the COVID-19 pandemic on interest in renal diseases

“…This increase reached statistical significance in the second period. Published studies highlighted the significantly higher prevalence of hypertension among COVID-19 patients (Esler and Esler 2020 ; Öztürk et al 2020 ; Fang et al 2020 ). Hypertension was the most frequent coexisting condition in the largest of several case series published during the COVID-19 outbreak from China (Guan et al 2020 ).…”

Correlation between interleukin gene polymorphisms and current prevalence and mortality rates due to novel coronavirus disease 2019 (COVID‐2019) in 23 countries

“…The pathogenesis of COVID‐19 harbors an effective inflammatory response, triggering a complex group of mediators including interleukins 3 . In the course of the disease, excessive production of pro‐inflammatory cytokines results in a cytokine storm which is responsible for the severe progression of the disease and the acute organ injuries 1 . The underlying mechanism is that SARS‐CoV‐2 can rapidly activate pathogenic T helper cell type 1 (Th1) cells to secrete pro‐inflammatory cytokines including interleukin‐6 (IL‐6), IL‐10, and IL‐17 4 .…”

“…Genetic polymorphisms implicated in understanding the basis of diseases also allow for the prevention of the spread of infections, and for the development of potentially effective treatments against the diseases. One common type of these polymorphisms, the single nucleotide polymorphisms (SNPs) are known to be effective in the pathways that play an important role in the attachment of the microbiological agent to the host cell, in the host's resistance to the diseases, in the susceptibility to disease and the severity of diseases 1 . There are growing numbers of reports stating that severe symptoms of COVID‐19 might be attributed to the human genetic variants in genes related to immune deficiency, pneumonia, sepsis, and/or cytokine storm 7 .…”

Angiotensin-converting enzyme gene insertion/deletion (I/D) polymorphism in Azerbaijan population

“…as well as in seasonal respiratory diseases (influenza, inflammation, etc.) (Abbasi et al, 2020;Bosso et al, 2020;Brojakowska et al, 2020;Cure E., Cumhur Cure M., 2020;Devaux et al, 2020;Guo et al, 2020;Hussain et al, 2020;Li et al, 2020;Lippi et al, 2020;Othman et al, 2020;Öztürk et al, 2020;South et al, 2020;Yamamoto et al, 2020;Zhang et al, 2020). The investigation of I/D polymorphism of ACE gene may help to understand molecular mechanisms of coronovirus infection.…”