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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

SO050

The IL1F10/IL1RN rs6734238 variant links HSV-1 exposure to inflammation in bipolar disorder: evidence for an immunogenetic pathway

IL1F10/IL1RN RS6734238 VARIANT LINKS HSV-1 EXPOSURE AND INFLAMMATION IN BIPOLAR DISORDER : EVIDENCE FOR AN IMMUNOGENETIC PATHWAY

In bipolar disorder, the rs6734238 G allele is associated with both HSV-1 seropositivity and elevated CRP and SAA levels, with HSV-1 infection amplifying rather than mediating this inflammatory effect.

The study aimed to investigate the interplay between IL-6-related genetic variants, infection exposure, and downstream inflammatory biomarkers in bipolar disorder (BD). In a French cohort of 342 individuals diagnosed with BD and 180 controls, three variants previously associated with IL-6 levels—rs660895 (HLA DRB1/5), rs6734238 (IL1F10/IL1RN), and rs4537545 (IL6R)—were genotyped using the TaqMan method. IL-6 pathway biomarkers (IL-6, CRP, TNF-α, VEGF, IL-17, SAA) were measured using the MSD technique, and serology for cytomegalovirus, herpes simplex virus type 1 (HSV-1), and Toxoplasma gondii was assessed to determine infection status; multiple linear regression, multinomial logistic regression, and mediation analysis were used. In the BD group, carriage of the rs6734238 G allele (AG+GG) was associated with elevated CRP and SAA levels and HSV-1 seropositivity; HSV-1-seropositive patients with BD had higher CRP, SAA, and VEGF levels. In the mediation model, the direct effect from the gene to inflammation was beta=0.49 (p=0.005), from the gene to CRP was beta=0.49 (p=0.004), and from HSV-1 infection to inflammation was beta=0.32 (p=0.04), whereas the pathway from the gene to HSV-1 infection (beta=0.14, p=0.08) and the indirect effect (beta=0.046, p=0.13) were not significant. In the interaction analysis, individuals who carried the G allele and were also HSV-1 seropositive had the highest risk of inflammation, defined as CRP above 3 mg/L; an adjusted RERI of 0.472 (95% CI −0.944 to 1.276) indicated a trend toward synergy. According to the authors, the rs6734238 polymorphism may identify a subgroup characterized by low-grade inflammation and increased susceptibility to HSV-1; the findings support a gene–environment interaction model and provide guidance for biological stratification and the development of targeted treatments.

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