ABSTRACT
The global coronavirus disease pandemic of 2019 (COVID-19) has changed humanity, affecting millions of people with and without various ailments. While the majority of COVID-19 patients recover, a significant percentage of patients experience serious problems, and some even die. The respiratory system, specifically the alveoli, is primarily affected by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) due to direct destruction of infected epithelial cells and the mimicked inflammatory response by the host, resulting in respiratory distress and, in some cases, cardiovascular complications At the same time, pregnant women, not simply the general population, are frequently affected by SARS-CoV-2 infection. As a result, viral infection is linked to higher levels of inflammatory biomarkers including interleukin-6 and dimer D, which could affect severe clinical aspects like thrombosis and cardiac damage. COVID-19-complications are more likely in patients with preexisting cardiovascular or cerebrovascular illness with risk factors such as male gender, elderly patients, hypertension, diabetes, obesity. As a result, these factors have been associated to an increased risk of morbidity and mortality. Although the connections between COVID-19 and cardiovascular inflammation in pregnant women require more exploration, this modest review focuses on the probable pathways by which SARS-CoV-2 infects its host, particularly in pregnant women with cardiovascular illness.
ABSTRACT
The advent of coronavirus-2019 (COVID-19) as a global pandemic has prompted scientists to address an urgent need to clarify the disease's pathogenic mechanisms and treatment. Severe acute respiratory syndrome is the severe complication of coronavirus 2 (SARS-CoV-2). This novel coronavirus uses the angiotensin 2 converting enzyme (ACE2) as a key target for cell surface attachment as well as a possible entry point into the host cell. Thus, for clinical intervention, a correct understanding of the elements that can influence the expression and function of ACE2 in the healthy and diseased body is critical. Over 60% of all persons in Europe have comorbidities, necessitating the usage of a prescription drug. While prior research has focused on the use of reninangiotensin inhibitors (RAS) to regulate ACE2 expression, new evidence in the literature suggests that a number of commonly used medicines for hypertension, heart failure, diabetes, and hyperlipidemia may interfere with COVID-19 infection. The involvement of the renin-angiotensinaldosterone system in the pathology of various complications such as hypertension and chronic kidney disease, through its aldosterone-releasing effects, stimulates coronary vasoconstriction, especially in the already ischemic heart. We offer a brief discussion of the methods through which medications that interfere with the renin-angiotensin system may influence the viral entrance of SARS-CoV-2 into cells, in addition to their known therapeutic effects.
ABSTRACT
Since the first cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, there have been challenges recognizing the clinical features of SARS‑CoV‑2 and identifying therapeutic options. This has been compounded by viral mutations that affect clinical response and primary epidemiological indicators. Multiple variants of SARS‑CoV‑2 have been identified and classified on the basis of nomenclature implemented by scientific organizations and the World Health Organisation (WHO). A total of five variants of concern (VOCs) have been identified to date. The present study aimed to analyse clinical and epidemiological features of each variant. Based on these characteristics, predictions were made about potential future evolution. Considering the time and location of SARS-CoV-2 VOC emergence, it was hypothesised that mutations were not due to pressure caused by the vaccines introduced in December 2020 but were dependent on natural characteristics of the virus. In the process of adapting to the human body, SARS-CoV-2 is expected to undergo evolution to become more contagious but less deadly. SARS-CoV-2 was hypothesized to continue spread through isolated epidemic outbreaks due to the unimmunized population, mostly unvaccinated children and adults, and for coronaviruses to continue to present a public health problem.