Abstract: In this study, we measured the frequency of revertants of a cytopathic strain of the duck hepatitis B virus that bears a single nucleotide substitution in the pre-S envelope protein open reading frame, resulting in the amino acid substitution G133E.
Abstract: Spontaneous revertants were found to be present at frequencies of 1 x 10(-5) to 6 x 10(-5) per G133E genome inoculated.
Abstract: Virus outgrowth was accompanied by a coselection of wild-type and spontaneous revertants during recovery of the ducklings from the acute liver injury caused by death of the G133E-infected cells.
Acute liver injury following infection with a cytopathic strain of duck hepatitis B virus.
Abstract: A single amino acid change of glycine to glutamic acid at position 133 (G133E) in the preS protein of duck hepatitis B virus (DHBV) caused an increase in the intranuclear pool of viral covalently closed circular DNA (cccDNA), resulting in a transient elevation of viral replication and eventual hepatocyte destruction.
Abstract: Birds infected with the G133E virus had increased periportal cellular proliferation and numerous lysed apoptotic hepatocytes following 100% infection of hepatocytes.
Abstract: In vivo viral infection with the G133E virus was compared with infection with wild-type virus over a 72-day period.
Abstract: The liver damage within G133E virus-infected birds subsided over time, resulting in mi
Competition in vivo between a cytopathic variant and a wild-type duck hepatitis B virus.
Abstract: In a mixed infection of ducklings with G133E and a small amount of wild-type virus, the wild-type virus was detected as the predominant genotype after recovery of normal liver histology.
Abstract: In vivo liver damage caused by this variant (G133E) occurred only during the first 2 weeks p.i., after which time cccDNA levels and liver histology returned to near normal despite continued virus replication.
Abstract: The results support the conclusion that the recovery from liver damage in G133E-infected ducklings was due to the emergence of spontaneous noncytopathic revertants rather than to host suppression of virus cytotoxicity.
Abstract: Two candidate revertant viral genomes were cloned directly from the serum virus of G133E-infected b
HBV mutation literature information.
PMID: 
2001
Journal of virology
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