ArticleJournal of multidisciplinary healthcare2025
No Genetic Causal Relationship between COVID-19 and Herpes Zoster: A Bidirectional Mendelian Randomization Analysis.
Article in Journal of multidisciplinary healthcare, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 authors.
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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.
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