Activity of adefovir dipivoxil against all patterns of lamivudine-resistant hepatitis B viruses in patients

C. E. Westland, H. Yang, W. E. Delaney IV, M. Wulfsohn, N. Lama, C. S. Gibbs, M. D. Miller, J. Fry, C. L. Brosgart, E. R. Schiff, Shelly Xiong

Research output: Contribution to journalArticlepeer-review

73 Scopus citations


One hundred and thirty-one post-liver transplantation patients with chronic hepatitis B and failing lamivudine therapy with detectable serum hepatitis B virus (HBV) deoxyribonucleic acid by hybridization assays or ≥1 × 106 copies/mL by polymerase chain reaction, and elevated alanine transaminase levels despite continuous lamivudine, were enrolled in an open-label study of adefovir dipivoxil. The B and C domains of HBV polymerase were sequenced for baseline samples to determine the presence of lamivudine resistance mutations. The results showed that 98% of the samples had tyrosine-methionine-aspartate-aspartate (YMDD) mutations, indicating a strong correlation between the above clinical definition of lamivudine treatment failure and the presence of YMDD mutations. In addition to the rtM204V/I and the rtL180M mutations, the mutation rtV173L was identified in 19% of patients. Four major patterns of lamivudine-resistant HBV were identified: rtL180M + rtM204V (60%), rtV173L + rtL180M + rtM204V (19%), rtM204I (9%) and rtL180M + rtM204I (9%). Treatment with adefovir dipivoxil showed similar antiviral efficacy in patients with lamivudine-resistant virus from all four patterns.

Original languageEnglish (US)
Pages (from-to)67-73
Number of pages7
JournalJournal of viral hepatitis
Issue number1
StatePublished - Jan 2005


  • Adefovir
  • Hepatitis B virus
  • Lamivudine
  • Liver
  • Mutation
  • Resistance
  • Transplantation

ASJC Scopus subject areas

  • Hepatology
  • Virology


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