title: 'e' antigen defective hepatitis B virus and course of chronic infection.
abstract: We studied the relations between HBV heterogeneity and different phases of HBV infection and disease in 145 HBsAg-positive carriers followed-up for 28 months (range 24-60 months). Viraemia was characterized for the relative prevalence of wild-type and HBeAg minus HBVs after HBV-DNA amplification by PCR using an oligonucleotide hybridization assay. HBeAg minus HBV was detected in 27% of immunotolerant HBV carriers, in 67% of patients with chronic hepatitis B (immunoelimination phase) and in 17% of HBsAg carriers with latent infection. Serum HBV-DNA and IgM anti-HBc became undetectable and ALT levels normalized, either spontaneously or after interferon therapy in 12 (36.3%) of 33 patients with an exclusive wild-type viraemia, but only in two (5.7%) of 35 patients with homogeneous HBeAg minus HBV (p = 0.005). An HBeAg minus viraemia higher than 20% was associated, in both HBeAg- and anti-HBe-positive patients, with HBV-induced liver disease and an unfavourable outcome of hepatitis. These findings suggest that surgence of HBeAg defective HBV is a virus strategy to survive under peculiar conditions dictated by the interplay between HBV and the host's immune system. The HBeAg/anti-HBe serological status is determined not only by the extent of virus replication and integration of HBV-DNA into cellular DNA but also by heterogeneity of HBV. The study of HBV heterogeneity in baseline sera of patients undergoing antiviral therapy appears to have a predictive value of the outcome of HBV infection in the single patient.
authors.affiliation: Department of Gastroenterology, Molinette Hospital, Turin, Italy.
authors.forename: M R
authors.initials: MR
authors.lastname: Brunetto
authors.forename: M
authors.initials: M
authors.lastname: Giarin
authors.forename: F
authors.initials: F
authors.lastname: Oliveri
authors.forename: G
authors.initials: G
authors.lastname: Saracco
authors.forename: C
authors.initials: C
authors.lastname: Barbera
authors.forename: T
authors.initials: T
authors.lastname: Parrella
authors.forename: M L
authors.initials: ML
authors.lastname: Abate
authors.forename: E
authors.initials: E
authors.lastname: Chiaberge
authors.forename: P L
authors.initials: PL
authors.lastname: Calvo
authors.forename: P
authors.initials: P
authors.lastname: Manzini
mesh_terms: D000328:Adult; D000367:Age Factors; D001483:Base Sequence; D002353:Carrier State; D002648:Child; D003673:Defective Viruses / Q000235:genetics* / Q000302:isolation & purification; D005260:Female; D005500:Follow-Up Studies; D006509:Hepatitis B / Q000276:immunology / Q000382:microbiology*; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006513:Hepatitis B e Antigens / Q000032:analysis / Q000235:genetics*; D006801:Humans; D007075:Immunoglobulin M / Q000032:analysis; D008297:Male; D008969:Molecular Sequence Data; D009838:Oligodeoxyribonucleotides; D014766:Viremia / Q000276:immunology / Q000382:microbiology
chemical_list: D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D007075:Immunoglobulin M; D009838:Oligodeoxyribonucleotides