Explore genetic susceptibility association between viral infections and Guillain-Barré syndrome risk using two-sample Mendelian randomization

• Published in: Journal of translational medicine 2024-10, Vol.22 (1), p.890-9, Article 890
• Main Authors: Kong, Qing-Xiang, Gao, Zhao-Kun, Liu, Yan, Jiang, Lu-Lu, Liu, Yuan-Jie, Lian, Zhi-Yun
• Format: Article
• Language: English
• Subjects: Analysis; Care and treatment; Development and progression; Diagnosis; Disease susceptibility; Epstein-Barr virus; Genetic aspects; Genetic Predisposition to Disease; Genetic susceptibility; Genome-Wide Association Study; Genomics; Guillain-Barre syndrome; Guillain-Barre Syndrome - genetics; Guillain-Barre Syndrome - virology; Guillain-Barré Syndrome; Health aspects; Hepatitis B; HIV (Viruses); Humans; Influenza; Medical research; Medicine, Experimental; Mendelian Randomization Analysis; Polymorphism, Single Nucleotide - genetics; Risk Factors; SARS-CoV-2 - genetics; Viral Infections; Virus diseases; Virus Diseases - complications; Virus Diseases - genetics
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-024-05704-8

Numerous observational studies have indicated that patients with Guillain-Barré syndrome (GBS) frequently had infections with various pathogens before the onset of the disease, particularly several viral infections. Some of these infections are linked to specific clinical and immunological subgroups of GBS, suggesting a potential correlation between viral infections and the development of GBS. However, observational studies have several limitations, including the presence of confounding factors. We explored the potential correlation between HIV, SARS-CoV-2, varicella-zoster virus, herpes simplex virus, Epstein-Barr virus, hepatitis B virus, and influenza virus with GBS using a two-sample Mendelian randomization approach. The data was derived from published summary statistics from genome-wide association studies (GWAS). After removing linkage disequilibrium, selecting strong instrumental variables and addressing confounding factors, we would conduct a two-sample Mendelian randomization analysis along with sensitivity testing and the MR-Steiger directional test. HIV may have a causal association with GBS (IVW: p = 0.010, OR [95% CI] 1.240 [1.052-1.463]), while no such relationship exists with COVID-19 (IVW: p = 0.275, OR [95% CI] 0.831[0.596-1.159]), varicella (IVW: p = 0.543, OR [95% CI] 0.919 [0.701-1.206]), herpes zoster (IVW: p = 0.563, OR [95% CI] 0.941 [0.766-1.156]), HSV (IVW: p = 0.280, OR [95% CI] 1.244 [0.837-1.851]), EBV (IVW: p = 0.218, OR [95% CI] 0.883 [0.724-1.076]), HBV (IVW: p = 0.179, OR [95% CI] 1.072 [0.969-1.187]), or influenza virus (IVW: p = 0.917, OR [95% CI] 0.971 [0.553-1.703]). We did not find any abnormal SNPs, pleiotropy, or heterogeneity, nor is there any reverse causation. Our study results indicate a causal relationship between HIV and GBS, providing new research directions for the etiology of GBS.