Mendelian randomization unveils genetic causal relationships between viral infections and systemic sclerosis

Mendelian randomization unveils genetic causal relationships between viral infections and systemic sclerosis

Abstract This study uses Mendelian randomization (MR) to investigate the potential causal relationships between viral infections, including Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), SARS-CoV-2, cytomegalovirus (CMV), human herpes virus 6 (HHV-6), varicella-zoster virus (VZV), her...

Full description

Saved in:
Bibliographic Details
Main Authors: Ting Cheng, He-Yi Zhang, Tian-Run Wang, Ruo-Lan Li, Zhi-Nan Jing, Yue-Hong Huo, Sheng-Xiao Zhang
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
Subjects:
Virus infection
Systemic sclerosis
Mendelian randomization
Causal relationship
Genome-wide association study
Online Access:https://doi.org/10.1038/s41598-025-08361-z
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract This study uses Mendelian randomization (MR) to investigate the potential causal relationships between viral infections, including Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), SARS-CoV-2, cytomegalovirus (CMV), human herpes virus 6 (HHV-6), varicella-zoster virus (VZV), herpes simplex virus (HSV), influenza A virus, and hepatitis B virus, and the risk of systemic sclerosis (SSc). Summary-level data on viral exposures and SSc outcomes were obtained from public genome-wide association studies (GWAS) databases. Causality was assessed using the inverse-variance weighted (IVW), MR-Egger, and weighted median methods. Sensitivity analysis was conducted to enhance the reliability and robustness of our findings. Genetically predicted anti-EBV viral capsid antigen IgG levels (OR = 3.400, 95% CI = 1.093–10.571, p = 0.035) were causally associated with an elevated risk of SSc, while HIV (OR = 0.787, 95% CI = 0.629–0.985, p = 0.037) and SARS-CoV-2 (OR = 0.335, 95% CI = 0.116–0.964, p = 0.043) correlated with a reduced risk of SSc. Sensitivity analysis validated the robustness of these associations (p > 0.05). Further elucidation of the underlying mechanisms by which EBV increases the risk of SSc could potentially identify interventions for promoting SSc prevention.
ISSN:2045-2322

Similar Items