The dysregulation of
cytokine production can lead to an inefficient immune response, promoting viral persistence that induces the progression of chronic viral
hepatitis. The study investigated the association of the
IL6-174G/C polymorphism with changes in
cytokine levels and its influence on the persistence and progression of
chronic hepatitis caused by HBV and HCV in 72 patients with
chronic hepatitis B (HBV), 100 patients with
hepatitis C (HCV), and a control group of 300 individuals. The genotyping of the
IL6-174G/C polymorphism was performed by real-time PCR, and
cytokine levels were measured by
enzyme-linked
immunosorbent assay (ELISA). HCV patients with the wild-type genotype (GG) had a higher viral load (p = 0.0230). The plasma levels of
IL-6 were higher among patients infected with HBV and HCV than among the control group (p < 0.0001). Patients with HCV were associated with increased inflammatory activity (A2−A3; p < 0.0001). In
hepatitis C, carriers of the GG genotype had higher levels of
IL-6 (p = 0.0286), which were associated with A2−A3 inflammatory activity (p = 0.0097). Patients with A2−A3 inflammatory activity and GG genotype had higher levels of
IL-6 than those with the GC/CC genotype (p = 0.0127). In conclusion, the wild-type genotype for the
IL6-174G/C polymorphism was associated with high levels of
IL-6 and HCV viral load and inflammatory activity, suggesting that this genotype may be a contributing factor to virus-induced
chronic infection.