Assessment and analysis of IL-8, IL-10, IL-12, IFN-γ and TNF-α in the Immunopathogenesis of Chronic Hepatitis B Virus Genotype D Infection

Abstract

Background: The pathogenesis of hepatitis B virus (HBV) infection is based on the interactions between HBV replication and immune responses. The aim of this study was to look into the immune-regulatory functions of IL-12, TNF-α, IFN-γ, IL-8, and IL-10 in chronic hepatitis B (CHB) genotype D infection at different serological stages. Materials and methods: The study included 125 chronic hepatitis cases. This research used a PCR-based genotyping method with type-specific primers. ELISA kit from Orgenium, Finland, measured TNF-α, IL-8, IL-10, and IL-12 levels, while ELISA, Diaclone, France, measured IFN-γ serum levels. Results: Genotype D was detected in 123 cases (98.4 %) out of 125 CHB patients. HBsAg and anti-HBcIgG were positive in all cases, 59 (47.96%) cases were positive for HBeAg. The median levels of IL-8, IL-10, and TNF-α were significantly higher in this study than in healthy controls, at 304.78±174.22 pg/ml, 13.74±6.15 pg/ml, and 180.75 ± 14.29 pg/ml, respectively. The amounts of IL-12 and IFN-γ were 19.25 pg/ml and 9.32 pg/ml, respectively. Conclusion: HBV infection may be persistent due to lopsided non-cytopathic antiviral mechanisms. Our findings suggest that lack of synchronicity of the cytokines may play a role in preventing non cytolytic elimination of the virus leading to chronicity. It's difficult to assign particular roles to any given cytokine in terms of HBV pathogenesis or clinical growth. Further research is necessary to further delineate the roles of individual cytokines.