Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
1.
Pharmacogenet Genomics ; 33(3): 41-50, 2023 04 01.
Article in English | MEDLINE | ID: covidwho-2279134

ABSTRACT

OBJECTIVE: The aim of the study was to investigate the gene polymorphisms of angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin type 1 receptor (AT1R) in association with coronavirus disease 2019 (COVID-19) mortality rates worldwide. METHODS: The prevalence of ACE I/D, AGT M235T, and AT1R A1166C alleles' frequencies in different populations was assessed. Data on COVID-19-related cases and deaths were acquired from the European Center for Disease Prevention and Control, which included weekly reports by country and continent. An Excel tool was developed to visualize the acquired data of mortality and incidence by classifying them by continent/country across specific periods of time. Spearman's nonparametric correlation was used to evaluate the association between country-based frequencies in RAS gene polymorphisms and COVID-19-related deaths. RESULTS: While China constituted the initial reservoir of COVID-19, incidence/mortality rates in Europe and America outnumbered the figures in the former. A clear association was identified between death rates and ACE D/I ( r = 0.3659; P = 0.033), as well as AGT A/G variants ( r = 0.7576; P = 0.015). Data on AT1R polymorphisms suggested no correlation with mortality rates. CONCLUSION: Our results demonstrated a significant disparity in COVID-19-related susceptibility and mortality among different populations and corroborate the importance of gene polymorphisms in predicting and consequently improving patients' outcomes.


Subject(s)
Angiotensinogen , COVID-19 , Peptidyl-Dipeptidase A , Humans , Angiotensinogen/genetics , China , COVID-19/genetics , COVID-19/mortality , Gene Frequency , Polymorphism, Genetic , Peptidyl-Dipeptidase A/genetics
2.
Mol Cell Biochem ; 476(4): 1891-1895, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1044487

ABSTRACT

Corona virus disease-19 (covid-19) is caused by a coronavirus that is also known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and is generally characterized by fever, respiratory inflammation, and multi-organ failure in susceptible hosts. One of the first things during inflammation is the response by acute phase proteins coupled with coagulation. The angiotensinogen (a substrate for hypertension) is one such acute phase protein and goes on to explain an association of covid-19 with that of angiotensin-converting enzyme-2 (ACE2, a metallopeptidase). Therefore, it is advisable to administer, and test the efficacy of specific blocker(s) of angiotensinogen such as siRNAs or antibodies to covid-19 subjects. Covid-19 activates neutrophils, macrophages, but decreases T-helper cells activity. The metalloproteinases promote the activation of these inflammatory immune cells, therefore; we surmise that doxycycline (a metalloproteinase inhibitor, and a safer antibiotic) would benefit the covid-19 subjects. Along these lines, an anti-acid has also been suggested for mitigation of the covid-19 complications. Interestingly, there are three primary vegetables (celery, carrot, and long-squash) which are alkaline in their pH-range as compared to many others. Hence, treatment with fresh juice (without any preservative) from these vegies or the antioxidants derived from purple carrot and cabbage together with appropriate anti-coagulants may also help prevent or lessen the detrimental effects of the covid-19 pathological outcomes. These suggested remedies might be included in the list of putative interventions that are currently being investigated towards mitigating the multi-organ damage by Covid-19 during the ongoing pandemic.


Subject(s)
COVID-19 Drug Treatment , Heart Failure/drug therapy , Inflammation/drug therapy , RNA, Small Interfering/therapeutic use , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Angiotensin-Converting Enzyme 2/genetics , Angiotensinogen/antagonists & inhibitors , Angiotensinogen/genetics , COVID-19/genetics , COVID-19/physiopathology , COVID-19/virology , Heart/drug effects , Heart/physiopathology , Heart/virology , Heart Failure/complications , Heart Failure/physiopathology , Heart Failure/virology , Humans , Inflammation/complications , Inflammation/genetics , Inflammation/virology , Neutrophils/virology , Pandemics , SARS-CoV-2/pathogenicity
SELECTION OF CITATIONS
SEARCH DETAIL