Abstract
Human herpes virus infection is thought to be associated with the development of vestibular neuritis (VN); however, the causal relationship is unclear. Large-scale genome-wide association studies were used in bidirectional Mendelian randomization (MR) analyses to evaluate the causal relationship between human herpes virus infections and VN in a cohort of 434,070 individuals. Inverse variance weighting, MR-Egger, and weighted median methods were used to estimate causality. These results were then validated through multiple sensitivity analyses. In forward MR inverse variance weighting analysis, genetically predicted herpes simplex virus (HSV) infections (odds ratio [OR] = 1.01; 95% confidence interval [CI]: 0.90-1.14; P = .814), HSV keratitis and keratoconjunctivitis (OR = 0.97; 95% CI: 0.87-1.08; P = .593), anogenital HSV infection (OR = 0.96; 95% CI: 0.87-1.06; P = .410), HSV-1 IgG (OR = 1.05; 95% CI: 0.59-1.88; P = .860), HSV-2 IgG (OR = 1.01; 95% CI: 0.90-1.14; P = .839), varicella-zoster virus infection (OR = 1.05; 95% CI: 0.97-1.14; P = .222), Epstein-Barr virus infection (OR = 1.00; 95% CI: 0.91-1.09; P = .944), and cytomegalovirus IgG (OR = 0.93; 95% CI: 0.79-1.10; P = .414), were not causally associated with VN. Moreover, no causality was found in the reverse MR analysis. Sensitivity analyses confirmed the reliability and validity of our findings. Our MR analysis revealed no significant causal effect of HSV-1, HSV-2, varicella-zoster virus, Epstein-Barr virus, and cytomegalovirus infections on the development of VN. These findings need to be further validated in larger, more diverse populations, and subgroup analyses will further reveal potential trends and differences in the study data.