ArticleScientific reports2025
Mendelian randomization unveils genetic causal relationships between viral infections and systemic sclerosis.
Article in Scientific reports, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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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.
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