‘e’ Antigen defective hepatitis B virus and course of chronic infection

• Published in: Journal of hepatology Vol. 13; pp. S82 - S86
• Main Authors: Brunetto, M.R., Giarin, M., Oliveri, F., Saracco, G., Barbera, C., Parrella, T., Abate, M.L., Chiaberge, E., Calvo, P.L., Manzini, P., Verme, G., Bonino, F.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Oxford Elsevier B.V 1991; Elsevier
• Subjects: Adult; Age Factors; Base Sequence; Biological and medical sciences; Carrier State; Child; Defective Viruses - genetics; Defective Viruses - isolation & purification; Female; Follow-Up Studies; Hepatitis B - immunology; Hepatitis B - microbiology; Hepatitis B e Antigens - analysis; Hepatitis B e Antigens - genetics; Hepatitis B Surface Antigens - analysis; Human viral diseases; Humans; Immunoglobulin M - analysis; Infectious diseases; Male; Medical sciences; Molecular Sequence Data; Oligodeoxyribonucleotides; Viral diseases; Viral hepatitis; Viremia - immunology; Viremia - microbiology
• ISSN: 0168-8278; 1600-0641
• DOI: 10.1016/0168-8278(91)90031-6

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 undectable 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.