Each phase of hepatitis B infection stimulates distinct viral kinetics and host immune responses resulting in liver damage and hepatic fibrosis. Our objective has been to correlate host inflammatory immune response including circulating Th1 and Th2 cytokines in patients with chronic hepatitis B infection with liver histopathology. Sixty-four patients with chronic hepatitis B without previous treatment were recruited. The liver histology and histological activity index were assessed for various degrees of necroinflammation and hepatic fibrosis. We determined circulating levels of the Th1 and Th2 cytokines. Forty-six males and 18 females at a median age of 34.5 years were studied. HBeAg was present in 28/64 (43.75%) of the patients. In patients negative for HBeAg, IL-10 and IFN-gamma were significantly correlated with degrees of necroinflammation ( , , resp.; ). Moreover, TNF-alpha was significantly correlated with degrees of fibrosis ( ; ), and IL-10 and TNF-alpha were significantly correlated with significant fibrosis ( , , resp.; ). These correlations were found in the HBeAg negative group as opposed to the HBeAg positive group. In HBeAg negative patients, circulating cytokines IL-10 and IFN-gamma were correlated with degrees of necroinflammation, whereas IL-10 and TNF-alpha were correlated with significant fibrosis. 1. Introduction Chronic hepatitis B infection is a major cause of chronic liver disease worldwide. Each phase of hepatitis B infection stimulates distinct viral kinetics and host immune responses resulting in liver damage and hepatic fibrosis [1]. Vaccine induced immune response in humans has provided excellent long term protection and result decline prevalence of hepatitis B virus (HBV) infection in long term [2, 3]. In contrast to host immune response in chronic hepatitis B infection, due to immune tolerance, only a small proportion of chronic hepatitis B (CHB) patients could clear the infection [4]. Histological damage and risk of HCC in CHB patients depend on various parameters such as duration of infection, coinfection with other hepatitis viruses, and alcohol consumption [5]. Cytokines are known to play a significant role in host immune responses. In chronic hepatitis B patients, the concentration of circulating Th17 cells (producing IL-17) increased with disease progression from CHB (mean, 4.34%) to acute-on-chronic liver failure (mean, 5.62%) patients as compared to healthy controls (mean, 2.42%) [6]. Furthermore, higher serum levels of IL-10 and IL-12 in HBeAg positive patients are correlated with early, spontaneous HBeAg
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