Hepatitis B Virus (HBV) e antigen (HBeAg), HBV DNA and precore mutations affecting HBeAg expression during active replication were studied in 72 Tunisian hepatitis B surface antigen (HBsAg) positive individuals: 30 asymptomatic carriers of the virus, 37 with chronic hepatitis and 5 with acute hepatitis. HBV DNA was detected in 44 patients, but only 20% of them expressed HBeAg. Precore mutant strains, with mutations at position 1896 or at positions 1896 and 1899, were detected by PCR-hybridization in 86 and 36% of patients, respectively. Wild-type strains were detected in 54% of patients. Precore mutants were found in chronically and in acutely infected individuals, in patients with severe and asymptomatic infections, in HBeAg positive as well as HBeAg negative individuals. These results show the high frequency of HBV precore mutants in Tunisia.

To determine the prevalence, as well as the clinical, virological and histological implications of GB virus C/hepatitis G virus (GBC-C/HGV) infection in patients with chronic hepatitis C virus (HCV) infection, sera from 671 well-characterized patients with chronic HCV infection were tested for GBV-C/HGV RNA using a sensitive and specific reverse transcription 'nested' polymerase chain reaction (RT-nPCR). GBV-C/HGV RNA was detected in 65 of 671 (9. 7%) patients with chronic HCV infection. Importantly, GBV-C/HGV co-infection was not associated with any changes in indices of liver diseases, including serum alanine transaminase levels, Knodell score or histology activity index (HAI). In this cohort, GBV-C/HGV co-infection was weakly associated with a shorter mean estimated duration of HCV infection and a higher median HCV viraemia level. We conclude that GBV-C/HGV has minimal or no impact on liver disease activity in patients with chronic HCV infection. This data supports the notion that GBV-C/HGV may not be a hepatitis virus.