A Specific IL6 Polymorphic Genotype Modulates the Risk of Trypanosoma cruzi Parasitemia While IL18, IL17A, and IL1B Variant Profiles and HIV Infection Protect Against Cardiomyopathy in Chagas Disease

摘要: Background Chagas disease caused by Trypanosoma cruzi (T. cruzi) affects approximately six million individuals worldwide. Clinical manifestations are expected to occur due the parasite persistence and host immune response. Herein we investigated potential associations between IL1B, IL6, IL17A, or IL18 polymorphism profiles cardiomyopathy T. parasitemia, as well impact of HIV infection on cardiopathy. Methods Two hundred twenty-six patients 90 control were analyzed. IL1B rs1143627 T>C, IL6 rs1800795 C>G, IL17A rs2275913 G>A, rs187238 rs1946518 C>A SNVs analyzed real-time PCR parasitemia PCR. Results Our data revealed association a cytokine gene never previously reported. The CG genotype lowered risk positive (OR = 0.45, 95% CI 0.24-0.86, P = 0.015). Original findings included AA s1946518 genotypes with decreased developing (OR = 0.27, 0.07-0.97, P = 0.044; OR = 0.35, 0.14-0.87, P = 0.023, respectively). TC associated reduced for severity, including NYHA (New York Heart Association) class ≥ 2 (OR = 0.21, 0.06-0.68, P = 0.009; OR = 0.48, 0.24-0.95, P = 0.036, respectively) LVEF (left ventricular ejection fraction) <45% (OR = 0.22, 0.05-0.89, P = 0.034). A novel, unexpected protective effect against development/progression was identified, based lower cardiopathy (OR = 0.48, 0.23-0.96, P = 0.039), (OR = 0.15, 0.06-0.39, P < 0.001), LVEF < 45% (OR = 0.03, 0.00-0.25, P = 0.001). Digestive involvement negatively NYHA ≥ 2 (OR = 0.20, 0.09-0.47, P < 0.001; OR = 0.24, 0.09-0.62, P = 0.004, Conclusions support role AA, modulatory in disease. Notably, shown protect cardiopathy, potentially synergistic highly active antiretroviral therapy (HAART), attenuating Th1-mediated response myocardium. This proposed hypothesis requires confirmation, however, larger more comprehensive future studies.