The association between viral infections and subacute thyroiditis (SAT) has been recognized, yet whether a genetic causal relationship exists between them remains unclear. To address this, we conducted a two-sample Mendelian randomization (MR) study to investigate this relationship. Genetic instruments for exposure to common viruses were derived from published genome-wide association study summary statistics. Inverse-variance weighted was the primary analysis, supplemented by MR-Egger and weighted median methods. Sensitivity analyses included tests for heterogeneity and horizontal pleiotropy. Results from our MR analysis indicated no statistically significant causal associations between SAT and the following viral exposures: herpes simplex virus (OR = 0.90, 95% CI = 0.73–1.10, P = .294), Epstein–Barr virus (OR = 1.03, 95% CI = 0.90–1.18, P = .63), cytomegalovirus immunoglobulin G (OR = 1.01, 95% CI = 0.74–1.38, P = .934), varicella-zoster virus (OR = 1.02, 95% CI = 0.90–1.15, P = .76), COVID-19 (OR = 1.02, 95% CI = 0.83–1.27, P = .821), hepatitis B virus (OR = 0.98, 95% CI = 0.94–1.03, P = .518), human immunodeficiency virus (OR = 1.02, 95% CI = 0.89–1.17, P = .778), influenza (OR = 0.96, 95% CI = 0.77–1.21, P = .747), measles (OR = 0.95, 95% CI = 0.85–1.06, P = .35), and mumps (OR = 1.00, 95% CI = 0.92–1.10, P = .914). All sensitivity analyses consistently supported the robustness of these findings. In summary, this study provides no evidence for a substantial causal effect of genetic liability to viral infections on SAT risk. Further research in larger and more diverse populations, ideally incorporating both genetic and temporal data on acute infections, is needed to comprehensively understand the role of viruses in SAT pathogenesis.
Zeng et al. (Fri,) studied this question.
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