analytical assessment of interleukin - 23 and -27 cytokines in healthy people and patients with hepatitis c virus infection (genotypes 1 and 3a)

background the immune system plays important roles in determining the outcomes of hepatitis c virus (hcv) infection. interleukin-23 and -27 (il-23 and il-27) are two novel il-12 cytokine family members known to enhance the t-lymphocyte response, but their precise involvement in hcv infection is not well known. objectives we investigated the serum il-27 and il-23 levels in patients with hcv infection and in healthy individuals. patients and methods in this case-control study, we assessed il-23 and il-27 levels in serum of 37 healthy individuals and 64 patients with chronic hcv using enzyme-linked immunosorbent assay (elisa). the relationship of cytokines level with liver enzymes (alt, ast, and alp), hcv genotype and viral load were analyzed. the differences of these cytokine levels in the groups of treatment and no treatment was compared. hcv genotypes were classified by hcv-specific primers methods. hcv rna loads were determined by fluorescence quantitative pcr. results serum level of il-23 was higher in hcv infected patients compared to control group (p = 0.005). however, no significant difference was seen in il-27 serum level between patients compared to the control group (p = 0.65). there was no significant difference in il-23 and il-27 level between genotype 1 hcv-infected- and 3a hcv-infected- patients. positive moderate correlation between il-23 and il-27 with viral load was found in type 3a and 1 hcv-infected patient. positive relative correlation was seen between alt and il-23 in 1a hcv-infected patients, which was higher than 3a hcv-infected patients; but there were no significant difference between serums liver enzymes with il-23 and il-27 in respect to genotype 3a and 1a hcv-infected patients conclusions these findings may reflect a vigorous pro-inflammatory reaction orchestrated by the host immune system against chronic hcv. also, a better understanding of the involvement mechanism considering the correlation between other genotypes with inflammatory cytokines in various stages of disease can be obtained.