Association of IL10 rs1800896 and IL33 rs10975519 with Severe COVID-19 Case Status in Iraqi Men: An Exploratory Case-Control Study

Host cytokine-gene variation may modify inflammatory responses to SARS-CoV-2, but evidence from Middle Eastern populations remains limited. This exploratory hospital-based case-control study evaluated IL10 rs1800896 and IL33 rs10975519 in 70 Iraqi men with quantitative PCR (qPCR)–confirmed severe COVID-19 and 30 qPCR-negative healthy male controls. Variants were genotyped by high-resolution melting, and ferritin, D-dimer and C-reactive protein (CRP) were measured. The two primary genotype-distribution tests used exact inference with Bonferroni correction; prespecified secondary genotype, inheritance-model and allele contrasts used exact odds ratios (ORs), 95% confidence intervals and false-discovery rate (FDR) adjustment. IL10 rs1800896 differed between groups (exact P = 0.0102; adjusted P = 0.0203; Cramer’s V = 0.304). The TC genotype, dominant C-carrier model and C allele met within-variant FDR criteria, although no secondary contrast remained below q < 0.05 when all 12 contrasts were adjusted jointly. IL33 rs10975519 showed no statistically supported variant-level association (exact P = 0.1112; Cramer’s V = 0.208). Ferritin, D-dimer and CRP were higher in severe cases (all P < 0.001). The IL10 finding is therefore a locus-level, hypothesis-generating association with severe-case versus healthy-control status, not evidence of causality or clinical prediction. Replication in larger, sex-balanced cohorts with infected non-severe comparison groups, validated genotyping and covariate-adjusted analyses is required.

Keywords: COVID-19; IL10; IL33; genetic association; biomarkers; Iraq.