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Background/aim: Occult hepatitis B virus (HBV) infection is characterized by the presence of HBV DNA in the absence of hepatitis B surface antigen (HBsAg) in the patient serum. Although such infections have been identified in patients with chronic hepatitis C, the clinical significance of those co-infections is still not understood. Our aim was, therefore, to assess the prevalence and clinical consequences of occult HBV infection in chronic hepatitis C patients undergoing antiviral therapy., Methods: The study population consisted of 53 HBsAg-negative patients with chronic hepatitis C treated with IFN/ribavirin or IFN/ribavirin/amantadine. Nine patients experienced a viral breakthrough (BT), 30 were non-responders (NR) and 14 were responders (R). HBV-DNA detection by PCR was performed using primers specific for the S region of the HBV genome and HCV-RNA detection by PCR with primers localised in both the 5'NC and core region of HCV genome, before, during and after treatment. Viral genome sequences were also studied., Results: Occult HBV genomes were found in the serum of four of 53 (7.5%) patients, unrelated to anti-HBc status. No significant differences in biochemical, virological, or histological markers, age, duration of infection, were observed in patients with or without HBV DNA. There was an inverse correlation in the evolution of HBV DNA and HCV RNA levels. Direct sequencing showed that S gene of occult HBV presented mutations in the "a" determinant while no specific mutation in the core region of HCV was observed. None of the four patients co-infected with HBV and HCV were responders to anti-HCV therapy., Conclusion: In our clinical setting, the prevalence of occult HBV co-infection among patients with chronic hepatitis C was low and independent of the presence of markers of previous HBV infection. Further studies in larger cohort of patients are warranted to determine if occult HBV co-infection may be involved in HCV resistance to combination therapy.

Background: Plasmacytoid dendritic cells (PDCs) are the major producers of interferon (IFN)- alpha within peripheral blood mononuclear cells (PBMCs)., Methods: We analyzed whether chronic hepatitis C virus (HCV) infection could be linked to a defective function or number of PDCs. We evaluated the capacity of PBMCs from 5 cohorts of subjects to produce IFN- alpha after viral stimulation. We concomitantly analyzed the frequency of PDCs and the levels of IFN- alpha transcripts within the PBMCs from the same cohorts., Results: PBMCs from patients with chronic HCV infection receiving antiviral therapy displayed a reduced capacity to release IFN- alpha, compared with those from healthy individuals, those from long-term responders to therapy, and those from nontreated patients. This defect was significantly correlated with the percentage of PDCs. In addition, PDCs from patients with chronic HCV infection receiving therapy displayed a reduced intrinsic capacity to produce IFN- alpha, which could be linked to the level of IFN- alpha transcripts., Conclusion: Our observations point to an effect of the therapy on either the survival or the localization of PDCs, rather than a direct detrimental effect due to the viral infection during chronic HCV infection.