Low frequency of precore hepatitis B virus mutants in anti-hepatitis B e—positive reactivation after loss of hepatitis B e antigen in patients with chronic hepatitis B

✍ Scribed by Marie Anne Loriot; Patrick Marcellin; Nathalie Talbodec; Véronique Guigonis; Michèle Gigou; Nathalie Boyer; Annie Bezeaud; Serge Erlinger; Jean Pierre Benhamou

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: English
• Weight: 611 KB
• Volume: 21
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840210304

✦ Synopsis

The objective of this study was to evaluate the role of hepatitis B virus (HBV) precore mutations in patients with anti-me-positive chronic hepatitis B with or without previous known HBe antigen (HBeAg) viremic phase, and to assess the potential implication of precore mutants in HBeAg-negative reactivation after loss of HBeAg. Nineteen patients were studied: 7 had a previous HBeAg-positive phase and had spontaneous or therapeutically induced loss of HBeAg (group A); 12 had no previous HBeAg-positive phase (group B). Direct sequencing of PCR products was performed on serum collected during the anti-mepositive phase in the two groups. In group A, precore sequencing showed that 5 patients were infected by wild-type virus, 1 patient was infected with a precore mutant, and 1 patient was found to be infected by a mixture of wild-type and precore mutant viruses. In group B, precore sequencing showed that only 1 patient was infected with wild-type virus and that 11 were infected with precore mutants. In a few patients, the presence of HBeAg within immune complexes may explain HBeAg negativity. In conclusion, our results show that, in patients with anti-HBe-positive chronic hepatitis B (1) precore mutations creating a stop codon are more frequently found in those without known previous HBeAg positivity; (2) after loss of HBeAg, the patients who have anti-HBepositive reactivation are infected by wild-type virus, which suggests that reactivation is not related to precore mutations; (3) HseAg negativity may be caused by immune complexes formation. (HEPATOLOGY 1995;21:627-631.) Abbreviations: HBeAg, hepatitis B e antigen; PCR, polymerase chain reaction; HRV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HBsAg, hepatitis B surface antigen.