One striking clinical feature of hepatitis C virus (HCV) infection is that more than 50% of patients with acute hepatitis C will develop chronic infection. To investigate its possible mechanisms, we examined the activation of type 2‐like T‐helper (Th2‐like) cells relating to the development of chronicity. Peripheral blood CD4+ T‐cell proliferation and cytokine secretion in response to a panel of recombinant HCV antigens including core (C22), envelope 1 (E1), E2, nonstructural (NS) protein 4 (C100), fusion protein of NS3 and NS4 (C200), and NS5 were assayed in 17 patients with acute hepatitis C. All six patients with self‐limited disease had a significant CD4+ T‐cell proliferation to C22, E1, C100, C200, and NS5, running parallel with the antigen‐stimulated secretion of interleukin (IL)‐2 and interferon γ (IFN‐γ), but not with interleukin (IL)‐4 and IL‐10, indicating predominant Th1 responses. Among the remaining 11 patients who developed chronicity, 6, 2, and 9 cases showed a specific CD4+ T‐cell response to C22, C100, and C200, respectively, and the responses were significantly lower than those of cases with recovery in terms of stimulation index (SI) (P < .05) and of antigen‐stimulated IL‐2 and IFN‐γ production. Importantly, IL‐4 and IL‐10 (Th2 responses) were detectable, and C22‐specific Th2‐like T‐cell clones could be generated from patients with chronicity. The data suggested that activation of Th2 responses in acute hepatitis C patients may play a role in the development of chronicity.

Background: Overweight and hepatic steatosis have been increasingly recognized recently. This study aimed to test whether substantial amount of fatty infiltration in liver, which may interfere with cytoplasmic distribution of hepatitis B surface antigen (HBsAg), can contribute to HBsAg seroclearance in HBsAg carriers. Methods: Clinical and laboratory data including ultrasound grading of hepatic steatosis were studied in 54 HBsAg carriers with HBsAg seroclearance, and the results were compared with 108 age-and sex-matched carriers with HBsAg persistence. Results: Body mass index and ultrasound grading of hepatic steatosis were significantly higher in HBsAg carriers with HBsAg seroclearance than in those with HBsAg persistence. The degrees of hepatic steatosis correlated significantly with body mass index (Po0.001). The prevalence of mild hepatic steatosis showed no significant difference (33% (18/54) vs 31% (33/108), P ¼ 0.72), but moderate-severe hepatic steatosis was significantly more prevalent in patients with HBsAg seroclearance (33% (18/54) vs 13% (17/108), P ¼ 0.01). HBsAg carriers with moderate and severe hepatic steatosis were associated with a 3.2-fold (95% confidence interval: 1.2-8.4, P ¼ 0.02) and 3.9-fold (95% confidence interval: 1.1-14.2, P ¼ 0.04), respectively, increased odds of HBsAg seroclearance compared to those without hepatic steatosis. Conclusion: Moderate-severe hepatic steatosis may contribute to HBsAg seroclearance in HBsAg carriers.

Patients with dual infection with hepatitis B virus (HBV) and delta virus (HDV) responded poorly to interferon (IFN) therapy. Little is known about the effect of IFN therapy in patients with HBV and hepatitis C virus (HCV) dual infection. The patients in two randomized controlled trials with chronic HBV infection were retrospectively assayed for HCV markers. The HBV responses to IFN therapy in patients with and without HCV markers were compared. An open trial was conducted in 4 patients who had lost their serum HBV surface antigen (HBsAg) but had continuing HCV viremia and hepatitis. Of the 15 patients seropositive for HCV marker(s), only 1 (6.7%) responded with seroclearance of HBV DNA and HBV e antigen, as compared with 46 (28%) of 164 HCV-negative patients (p = 0.058). Icteric hepatitis developed in 1 patient on emergence of serum HCV RNA in association with seroclearance of HBV DNA. In contrast, good response was demonstrated in 3 of the 4 patients who had lost serum HBsAg before therapy. The results suggest that IFN therapy is not only of limited value in patients with dual infection with HBV and HCV but also has a potential risk of severe hepatitis if the clearance of one virus removes its suppressive effect on and facilitates the emergence of the other. However, patients with continuing HCV hepatitis after termination of the chronic HBsAg carrier state responded well to IFN therapy.

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