Clonal evolution of hepatitis B virus polymerase gene mutations during lamivudine-adefovir combination treatment

World J Gastroenterol. 2012 Nov 28;18(44):6437-46; discussion p.6445. doi: 10.3748/wjg.v18.i44.6437.

Abstract

Aim: To identify hepatitis B virus polymerase gene mutations during antiviral therapy using lamivudine-adefovir sequential monotherapy followed by lamivudine-adefovir combination therapy.

Methods: The patient cohort included four adult chronic hepatitis B patients who had undergone sequential monotherapy, first with lamivudine (LMV) and then, after developing viral breakthrough, with adefovir (ADV) therapy. All of the patients had non-response or viral breakthrough after LMV-ADV sequential monotherapy, which resulted in the switching of their antiviral regimen to LMV-ADV combination therapy. Eleven serum samples from the four patients who showed non-response to rescue LMV-ADV combination therapy were collected sequentially at a time before the antiviral treatment and then during the LMV monotherapy, ADV monotherapy, and LMV-ADV combination therapy. For the genotypic analysis, the whole 1310-bp polymerase gene region was amplified, cloned and sequenced.

Results: All patients had been previously treated with 100 mg of LMV once daily for a 15- to 26-mo period. The emergence of resistance mutations to LMV, such as rtM204V/I and/or rtL180M, were found in all patients. Their antiviral regimens were switched to ADV monotherapy as the second line treatment. All patients had viral breakthrough or non-response after the LMV-ADV sequential monotherapy. ADV-resistant mutations were detected after 13 to 19 mo of LMV-ADV sequential monotherapy. The rtA181V/T mutations were predominantly identified during the ADV treatment in the LMV-resistant patients. Twenty-seven of 38 clones were combined with an amino acid change at rt181; three clones had mutations in rt236 and one clone had a combined mutation. The rtA181V/T mutations were not suppressed by the LMV-ADV combination therapy. Thirty-nine of 64 clones showed an rtA181V/T mutation and six clones showed combined mutations in rt181 and rt236. Mutations in rt204 re-emerged during the combination treatment. The rt181 and rt204 mutations did not co-exist in one clone.

Conclusion: Add-on lamivudine therapy with adefovir for adefovir resistance may not suppress the pre-existing adefovir-resistant mutation that develops during lamivudine-adefovir sequential monotherapy.

Keywords: Adefovir; Drug resistance; Hepatitis B virus; Lamivudine; Mutation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenine / analogs & derivatives*
  • Adenine / therapeutic use
  • Adult
  • Antiviral Agents / therapeutic use*
  • Clonal Evolution*
  • Drug Combinations
  • Drug Resistance, Viral / genetics
  • Drug Substitution
  • Gene Products, pol / genetics*
  • Genotype
  • Hepatitis B virus / drug effects*
  • Hepatitis B virus / enzymology
  • Hepatitis B virus / genetics
  • Hepatitis B, Chronic / diagnosis
  • Hepatitis B, Chronic / drug therapy*
  • Hepatitis B, Chronic / virology
  • Humans
  • Lamivudine / therapeutic use*
  • Male
  • Middle Aged
  • Mutation*
  • Organophosphates / therapeutic use*
  • Organophosphonates / therapeutic use*
  • Phenotype
  • Time Factors
  • Treatment Outcome

Substances

  • Antiviral Agents
  • Drug Combinations
  • Gene Products, pol
  • Organophosphates
  • Organophosphonates
  • P protein, Hepatitis B virus
  • lamivudine-adefovir combination
  • Lamivudine
  • adefovir
  • Adenine