{"title":"No Genetic Causal Relationship between COVID-19 and Herpes Zoster: A Bidirectional Mendelian Randomization Analysis.","authors":"Yuan Cao, Xinhua Hu, Jun Li, Yumin Zheng","doi":"10.2147/JMDH.S518008","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Increased incidences of herpes zoster (HZ) have been reported among COVID-19 patients, but the underlying causal mechanisms remain unclear. Inspired by an atypical case of HZ in a COVID-19 patient, we conducted a bidirectional Mendelian randomization (MR) analysis to investigate potential causal relationships.</p><p><strong>Patients and methods: </strong>The genetic statistics were extracted from the COVID19-hg GWAS meta-analyses and the IEU GWAS database. MR analyses were performed using the inverse-variance weighted (IVW) method as the primary approach, with MR-Egger, weighted median, simple mode, and weighted mode methods as supplementary strategies. Heterogeneity and pleiotropy were assessed using Cochran's Q test, MR-Egger intercept, and MR-PRESSO analysis, while outliers were evaluated with MR-radial plots.</p><p><strong>Results: </strong>The MR analysis did not support a significant causal relationship between COVID-19 and HZ. In the forward analysis, the IVW method revealed no significant associations between COVID-19 susceptibility (β = -0.053, SE = 0.182, P = 0.77), hospitalization (β = 0.060, SE = 0.069, P = 0.38), or severity (β = 0.015, SE = 0.048, P = 0.75) and HZ. Similarly, the reverse analysis showed no significant effect of HZ on COVID-19 susceptibility (β = 0.006, SE = 0.006, P = 0.33), hospitalization (β = -0.012, SE = 0.012, P = 0.32), or severity (β = -0.015, SE = 0.020, P = 0.46). Sensitivity analyses confirmed these findings, showing no substantial heterogeneity or horizontal pleiotropy.</p><p><strong>Conclusion: </strong>Our findings provide no evidence of a causal relationship between genetic predisposition to COVID-19 and the risk of HZ reactivation. The observed clinical association may be attributable to non-genetic factors, such as immune suppression or stress related to COVID-19 and its treatment. Further studies are warranted to explore these alternative mechanisms and improve clinical management of HZ in the context of COVID-19.</p>","PeriodicalId":16357,"journal":{"name":"Journal of Multidisciplinary Healthcare","volume":"18 ","pages":"2957-2967"},"PeriodicalIF":2.4000,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126108/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Multidisciplinary Healthcare","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2147/JMDH.S518008","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"HEALTH CARE SCIENCES & SERVICES","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: Increased incidences of herpes zoster (HZ) have been reported among COVID-19 patients, but the underlying causal mechanisms remain unclear. Inspired by an atypical case of HZ in a COVID-19 patient, we conducted a bidirectional Mendelian randomization (MR) analysis to investigate potential causal relationships.
Patients and methods: The genetic statistics were extracted from the COVID19-hg GWAS meta-analyses and the IEU GWAS database. MR analyses were performed using the inverse-variance weighted (IVW) method as the primary approach, with MR-Egger, weighted median, simple mode, and weighted mode methods as supplementary strategies. Heterogeneity and pleiotropy were assessed using Cochran's Q test, MR-Egger intercept, and MR-PRESSO analysis, while outliers were evaluated with MR-radial plots.
Results: The MR analysis did not support a significant causal relationship between COVID-19 and HZ. In the forward analysis, the IVW method revealed no significant associations between COVID-19 susceptibility (β = -0.053, SE = 0.182, P = 0.77), hospitalization (β = 0.060, SE = 0.069, P = 0.38), or severity (β = 0.015, SE = 0.048, P = 0.75) and HZ. Similarly, the reverse analysis showed no significant effect of HZ on COVID-19 susceptibility (β = 0.006, SE = 0.006, P = 0.33), hospitalization (β = -0.012, SE = 0.012, P = 0.32), or severity (β = -0.015, SE = 0.020, P = 0.46). Sensitivity analyses confirmed these findings, showing no substantial heterogeneity or horizontal pleiotropy.
Conclusion: Our findings provide no evidence of a causal relationship between genetic predisposition to COVID-19 and the risk of HZ reactivation. The observed clinical association may be attributable to non-genetic factors, such as immune suppression or stress related to COVID-19 and its treatment. Further studies are warranted to explore these alternative mechanisms and improve clinical management of HZ in the context of COVID-19.
目的：报道了COVID-19患者中带状疱疹（HZ）的发病率增加，但潜在的因果机制尚不清楚。受2019冠状病毒病患者非典型HZ病例的启发，我们进行了双向孟德尔随机化（MR）分析，以探讨潜在的因果关系。患者和方法：遗传统计数据提取自covid - 19-hg GWAS荟萃分析和IEU GWAS数据库。MR分析以反方差加权（IVW）法为主要方法，MR- egger法、加权中位数法、简单模式法和加权模式法作为补充策略。异质性和多效性采用Cochran’s Q检验、MR-Egger截距和MR-PRESSO分析进行评估，异常值采用MR-radial图进行评估。结果：MR分析不支持COVID-19与HZ之间存在显著的因果关系。在前瞻性分析中，IVW方法显示COVID-19易感性（β = -0.053, SE = 0.182, P = 0.77）、住院率（β = 0.060, SE = 0.069, P = 0.38）或严重程度（β = 0.015, SE = 0.048, P = 0.75）与HZ无显著相关性。同样，反向分析显示，HZ对COVID-19易感性（β = 0.006, SE = 0.006, P = 0.33）、住院率（β = -0.012, SE = 0.012, P = 0.32）或严重程度（β = -0.015, SE = 0.020, P = 0.46）无显著影响。敏感性分析证实了这些发现，显示没有实质性的异质性或水平多效性。结论：我们的研究结果没有证据表明COVID-19遗传易感性与HZ再激活风险之间存在因果关系。观察到的临床关联可能归因于非遗传因素，例如与COVID-19及其治疗相关的免疫抑制或压力。需要进一步的研究来探索这些替代机制，并在COVID-19背景下改善HZ的临床管理。
期刊介绍：
The Journal of Multidisciplinary Healthcare (JMDH) aims to represent and publish research in healthcare areas delivered by practitioners of different disciplines. This includes studies and reviews conducted by multidisciplinary teams as well as research which evaluates or reports the results or conduct of such teams or healthcare processes in general. The journal covers a very wide range of areas and we welcome submissions from practitioners at all levels and from all over the world. Good healthcare is not bounded by person, place or time and the journal aims to reflect this. The JMDH is published as an open-access journal to allow this wide range of practical, patient relevant research to be immediately available to practitioners who can access and use it immediately upon publication.
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