Abstract: Subsequent to the instigation of antiviral therapy, the dominant drug resistant HBV which caused virological breakthrough and was associated with hepatic failure displayed a series of unique mutations particularly in the BCP (A1762T and G1764A) and in the polymerase (rtL180M, rtM204V, rtA222T and rtL336V), core (cP5T, cS26A,
Reduced antigenicity of the hepatitis B virus HBsAg protein arising as a consequence of sequence changes in the overlapping polymerase gene that are selected by lamivudine therapy.
Abstract: HBsAg mutants including E164D, W196S, I195M, M198I, and E164D/I195M (corresponding to the polymerase protein changes of V519L, M550I, L526M/M550V V553I, and V519L/L526M/M550V) selected during lamivudine treatment also demonstrated reduced binding to anti-HBs antibody.
HBV mutation literature information.
PMID: 
2003
Journal of clinical virology
Browser Board
Co-occurred Entities
Filtrator