Evidence map›Paper›PMID 39506873›Full record

ArticleVirology journal2024

The causal association between COVID-19 and ischemic stroke: a mendelian randomization study.

Zhaojie Zhang, Jie Hua, Liang Chen

Abstract read
In one paragraph

Article in Virology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Zhaojie ZhangDepartment of Critical Care Medicine, Zhongda Hospital Lishui Branch, Nanjing Lishui People's Hospital, Southeast University, Nanjing, 211200, China.
Jie HuaDepartment of Gastroenterology, Jiangsu Province People' s Hospital, Nanjing, 211029, China.
Liang ChenDepartment of Infectious Diseases, Taikang Xianlin Drum Tower Hospital, Affiliated Hospital of Medical College of Nanjing University, NO 188 Lingshan North Road, Qixia District, Nanjing, 210046, China. Chenliang1995@sina.com.

Funding

Nanjing Medical Science and Technology Development Fund NO. YKK22239
6 · The paper itself

Abstract

backgroundCurrent observational data indicates that ischemic stroke (IS) affects a significant proportion of people with COVID-19. The current study sought to evaluate the causal relationship between COVID-19 and IS.

methodsA two-sample Mendelian randomization (2 S-MR) approach was used to probe the relationship between genetic determinants of three COVID-19 parameters (SARS-CoV-2 infection, COVID-19 hospitalization, and severe COVID-19) and the incidence of IS based on genome-wide association studies (GWAS) data. Using this 2 S-MR technique, expression quantitative trait loci (eQTL) and GWAS studies were further assessed for overlap to identify common causative genes associated with severe COVID-19 and IS.

resultsIVW approaches indicated the genetic variants linked to COVID-19 hospitalization (OR 1.04, 95% CI 1.01-1.08, p = 0.023) and severe COVID-19 (OR 1.03, 95% CI 1.01-1.05, p = 0.007) were both significantly linked to greater odds of IS. In contrast, there was no causal association between genetic SARS-CoV-2 infection susceptibility and the occurrence of IS (OR 0.99, 95% CI 0.92-1.06, p = 0.694). Ten shared causal genes (TNFSF8, CFL2, TPM1, C15orf39, LHFPL6, FAM20C, SPAG9, KCNJ2, PELI1, and HLA-L) were established as possible mediators of the interplay between severe COVID-19 and the development of IS, with these genes primarily being enriched in immune-related and renin-angiotensin-aldosterone system pathways.

conclusionThese findings indicate a possible causative relationship between IS risk and COVID-19 severity, offering crucial new information for managing COVID-19 patients. Promising options for therapeutic therapies for severe COVID-19 complicated by IS include the common genes found in the present study.

Indexed as

COVID-19Genome-Wide Association StudyIschemic StrokeMendelian Randomization AnalysisQuantitative Trait LociSARS-CoV-2Genetic Predisposition to DiseaseHospitalizationHumansPolymorphism, Single NucleotideCausal effectCausal geneCOVID-19 hospitalizationIschemic strokeMendelian randomizationSARS-CoV-2 infectionSevere COVID-19

Identifiers

PMID39506873
PMCPMC11542230

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LicenceCC BY-NC-ND
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.