Journal article

Effect of the G1896A precore mutation on drug sensitivity and replication yield of lamivudine-resistant HBV in vitro

RYM Chen, R Edwards, T Shaw, D Colledge, WE Delaney, H Isom, S Bowden, P Desmond, SA Locarnini

Hepatology | W B SAUNDERS CO | Published : 2003

Abstract

Hepatitis B e antigen (HBeAg) negative chronic hepatitis B (CHB) is frequently caused by a mutation (G1896A) in the hepatitis B virus (HBV) precore (PC) reading frame that creates a stop codon, causing premature termination of the PC protein. During lamivudine treatment, drug resistance develops at a similar rate in HBeAg positive and HBeAg negative CHB. Lamivudine-resistant HBV mutants have been shown to replicate inefficiently in vitro in the absence of PC mutations, but it is unknown whether the presence of PC mutations affects replication efficiency or antiviral sensitivity. This study utilized the recombinant HBV baculovirus system to address these issues. HBV baculoviruses encoding the..

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