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Interleukin (IL)-12 plays an essential role in host defense against infectious diseases. Serum IL-12 concentration and blood mononuclear cell production with or without specific interferon (IFN)-γ priming were investigated in 65 chronic hepatitis C virus (HCV) patients and 25 healthy donors. HCV patients had higher serum IL-12 levels (P = .004) and produced higher amounts after IFN-γ priming (P < .001) than donors. A subset of patients did not produce IL-12: They had lower serum levels (P = .032) and showed signs of liver piecemeal necrosis less frequently (P = .011). Patients with greater liver necroinflammatory activity produced more IL-12 than patients with minimal or mild activity and donors (P < .01). During IFN-α therapy for 16 HCV patients, individuals with end-of-treatment alanine aminotransferase normalization and clearance of viremia had higher serum levels and produced more IL-12 than those who did not (P < .05). These results suggest a role for IL-12 in the immunopathogenesis and outcome of HCV infection. [ABSTRACT FROM PUBLISHER]

Antibody responses to the GOR epitope and hepatitis C virus (HCV) core were investigated in 136 patients with chronic HCV infection. Patient age (P = .011) and necroinflammatory activity (P < .001) were significantly greater in 92 (67.6%) patients with anti-GOR than in 44 (32.4%) patients without anti-GOR. HCV RNA concentration was significantly higher in patients with anti-GOR (P = .031). HCV la or Ib genotypes were also found according to anti-GOR status. GOR and HCV core (amino acids 5–19) antibody responses correlated significantly (rs = .615, P < .001). Anti-HCV core(5–19) was detected in 67 (73%) of 92 patients with and in 14 (32%) of 44 without anti-GOR (P < .001). Patients with concurrent anti-GOR and anti-HCV core(5–19) had significantly greater necroinflammatory activity (P = .003). By multivariate analysis, anti-HCV core(5–19), patient age, and necroinflammatory activity were correlated with anti-GOR response (P < .001). Reactivity to the GOR autoepitope correlates with HCV core response and liver necroinflammatory activity, thus suggesting an immunopathogenic role in chronic hepatitis C. [ABSTRACT FROM PUBLISHER]

IgM anti-hepatitis C virus (HCV) and HCV RNA were longitudinally tested for 4.0–8.7 years in 40 patients with chronic HCV infection. Patients in disease remission usually lost IgM antiHCV and HCV RNA, but most patients experiencing disease reactivation had increased levels of the IgM antibody or it reappeared before the biochemical relapse, even when HCV RNA was undetectable. IgM anti-HCV was detectable in most patients with ongoing viral replication and persistent liver disease. Despite long-term disease remission, IgM anti-HCV may persist and be detectable with or without evidence of serum HCV RNA; this indicates a possible disease reactivation, which could occur after several years of sustained transaminase normalization. Detection of IgM anti-HCV in chronic hepatitis C indicates an active immune response to persistent viral infection and should, therefore, be considered as a sensitive marker of active HCV replication and HCV-associated liver disease. [ABSTRACT FROM PUBLISHER]

Examines the induction of MxA protein in peripheral blood mononuclear cells in patients infected with hepatitis C virus. Activation of interferon system to viral infection; Use of immunoblot assay in the detection of human MxA protein; Differences in the immunoregulatory mechanisms between chronic hepatitis B and C.