Abstract:Coronavirus disease 2019 (COVID-19) is an acute infection of the respiratory tract that emerged in December 2019 in Wuhan, China. It was quickly established that both the symptoms and the disease severity may vary from one case to another and several strains of SARS-CoV-2 have been identified. To gain a better understanding of the wide variety of SARS-CoV-2 strains and their associated symptoms, thousands of SARS-CoV-2 genomes have been sequenced in dozens of countries. In this article, we introduce COVIDomic,… Show more
“…As further research directions, we aim to apply the same model using different feature extraction methods according to the sequence and the structure of the proteins to obtain more detailed biological information about the virus behavior and its infection cycle. Other classification methods will also be explored in future studies such as principal components analysis and its new derivations, including supervised and unsupervised approaches, as well as functional data analysis, partial least squares structures, and other recent methodologies [ [36] , [37] , [38] , [39] , [40] , [41] , [46] , [47] , [48] , [49] ].…”
Section: Discussion and Conclusion Limitations And Future Researchmentioning
“…As further research directions, we aim to apply the same model using different feature extraction methods according to the sequence and the structure of the proteins to obtain more detailed biological information about the virus behavior and its infection cycle. Other classification methods will also be explored in future studies such as principal components analysis and its new derivations, including supervised and unsupervised approaches, as well as functional data analysis, partial least squares structures, and other recent methodologies [ [36] , [37] , [38] , [39] , [40] , [41] , [46] , [47] , [48] , [49] ].…”
Section: Discussion and Conclusion Limitations And Future Researchmentioning
“… / Nextstrain https://nextstrain.org/ Virus information (including influenza virus, SARS-CoV-2, dengue virus, Zika virus, Monkeypox, Ebola virus, etc.) [5] NCBI Influenza Virus Database https://www.ncbi.nlm.nih.gov/genomes/FLU/Database/nph-select.cgi?go = database Influenza virus information / NCBI SARS-CoV-2 Resources https://www.ncbi.nlm.nih.gov/sars-cov-2/ SARS-CoV-2 Information / UniProt https://www.uniprot.org/ Contains virus related proteins information [8] AlphaFold https://alphafold.com/ Contains structural biological information of virus / COVIDomic https://covidomic.com/ Multi-omics health data of COVID-19 patients Clinical data [6] ClinicalTrials.gov https://clinicaltrials.gov/ct2/home Clinical data / FluReassort https://www.jianglab.tech/FluReassort Genomic reassortments of influenza virus Database for specific studies [9] EpiGraphDB https://epigraphdb.org Contains epidemiological data on diseases caused by various viral infections Epidemiological data [11] KGCoV https://www.biosino.org/kgcov/ SARS-CoV genome-epidemiological knowledge graph [12] CoV-AbDab https://opig.stats.ox.ac.uk/webapps/covabdab/ Information on structures of coronavirus antibodies Immunology related information <...…”
Section: Database Of Emerging Infectious Virusesmentioning
confidence: 99%
“…Nextstrain, developed by James Hadfield et al [5] includes several virus-related information, with the most significant feature of using system dynamics analysis technology to generate a phylogenetic tree of the virus and collect spatiotemporal information when the data is updated, presenting a spatiotemporal view of the evolution and transmission of the virus to users. COVIDomic developed by Naumov et al [6] is a multiomics online platform that collects large amounts of health data from COVID-19 patients to determine the origin of the virus and the expected severity of the disease by analyzing multimodal genomic data from these patients. In addition, websites such as National Center for Biotechnology Information (NCBI) and European Nucleotide Archive collect genomic information on many viruses, while the platforms like Protein Data Bank (PDB) [7] , UniProt [8] , and AlphaFold collect the structural biology and protein information of viruses.…”
Section: Database Of Emerging Infectious Virusesmentioning
“…While a growing body of research has identi ed genetic loci associated with COVID-19 susceptibility and severity, the precise relationship between these genetic markers and adverse outcomes in COVID-19 patients remains less clear 6, [23][24][25] . From a biological standpoint, although QT interval prolongation may be associated with SARS-CoV-2-induced myocarditis and changes in physiological parameters such as electrolytes and hormones 7,26 , the observational and cross-sectional nature of these studies, coupled with the complexity of this relationship in uenced by multiple factors, leaves us uncertain as to whether a genuine causal association exists between SARS-CoV-2 infection and QT interval prolongation.…”
Background
QT interval, a vital marker of ventricular electrical activity during depolarization and repolarization, garnered significant attention during the COVID-19 pandemic. However, it remains unclear whether COVID-19 directly affects QT interval prolongation. This study leverages Mendelian randomization (MR) to investigate the genetic causation between COVID-19 and QT interval alterations.
Methods
In over 1000,000 individuals of European ancestry, genetic proxies representing three COVID-19 phenotypes (COVID-19, hospitalized COVID-19, and severe COVID-19), were identified under the primary MR assumption, and serve as instrumental variables (IVs). Genetic causal effects of COVID-19 on QT intervals from 84,630 UK Biobank participants were inferred using univariate two-sample MR (TSMR) and multi-exposure-adjusted multivariate MR (MVMR). MR-RAPS method and radial MR frame were used to provide robustness and outlier variant detection for effect assessment, and sensitivity analysis was further applied to detect the presence of horizontal pleiotropy.
Results
Independent 15, 33, and 29 IVs were used in COVID-19, hospitalized COVID-19, and severe COVID-19, respectively. Univariate TSMR analyses showed non-significant causal effect estimates between COVID-19 and the QT interval across all COVID-19 phenotypes. MR-RAPS and outlier-corrected radial MR analyses further supported this null causal estimation. In confounder-adjusted MVMR analysis, this nonsignificant causality was independent of BMI, smoking, and alcohol consumption. Sensitivity analyses failed to reveal any evidence of bias arising from horizontal pleiotropy, abnormal data distribution, or weak instruments.
Conclusions
Genetically, COVID-19 is not causally associated with QT interval prolongation. Inconsistent findings in observational research may be attributed to residual confounding.
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