RG7128 alone or in combination with pegylated interferon-α2a and ribavirin prevents hepatitis C virus (HCV) Replication and selection of resistant variants in HCV-infected patients

J Infect Dis. 2010 Nov 15;202(10):1510-9. doi: 10.1086/656774. Epub 2010 Oct 13.

Abstract

Introduction: RG7128 (prodrug of PSI-6130) shows potent antiviral efficacy in patients infected with hepatitis C virus (HCV) genotypes 1, 2, or 3, with mean viral load decreases of 2.7 and 5 log(10) IU/mL, respectively, associated with 1500-mg doses twice daily after monotherapy for 2 weeks and with 1000-mg and 1500-mg doses twice daily after treatment in combination with the standard of care (SOC) for 4 weeks.

Results: From 32 patients treated with RG7128 monotherapy for 2 weeks, marginal viral load rebound was observed in 3 HCV genotype 1-infected patients, whereas partial response was observed in 2 genotype 1-infected patients. From 85 patients receiving RG7128 in combination with SOC, 1 HCV genotype 1-infected patient experienced a viral rebound, and 2 genotype 3-infected patients experienced a transient rebound. Five genotype 1-infected patients had an HCV load of >1000 IU/mL at the end of 4-week treatment. No viral resistance was observed, per NS5B sequencing and phenotypic studies. PSI-6130 resistance substitution S282T needs to be present at levels of ≥90% within a patient's quasispecies to confer low-level resistance. No evidence of S282T was found by population or clonal sequence analyses.

Conclusions: The requirement for a predominant S282T mutant quasispecies, its low replication capacity, and the low-level resistance it confers probably contribute to the lack of RG7128 resistance observed in HCV-infected patients.

Publication types

  • Multicenter Study
  • Randomized Controlled Trial

MeSH terms

  • Amino Acid Substitution
  • Antiviral Agents / pharmacology
  • Antiviral Agents / therapeutic use*
  • Deoxycytidine / analogs & derivatives*
  • Deoxycytidine / pharmacology
  • Deoxycytidine / therapeutic use
  • Drug Resistance, Viral / genetics
  • Drug Therapy, Combination
  • Hepacivirus / drug effects*
  • Hepacivirus / genetics
  • Hepacivirus / physiology
  • Hepatitis C, Chronic / drug therapy*
  • Hepatitis C, Chronic / virology
  • Humans
  • Interferon alpha-2
  • Interferon-alpha / therapeutic use*
  • Neuseeland
  • Polyethylene Glycols / therapeutic use*
  • Recombinant Proteins
  • Ribavirin / therapeutic use*
  • Selection, Genetic
  • Vereinigte Staaten
  • Viral Load
  • Viral Nonstructural Proteins / genetics
  • Virus Replication / drug effects

Substances

  • 2'-fluoro-2'-methyl-3',5'-diisobutyryldeoxycytidine
  • Antiviral Agents
  • Interferon alpha-2
  • Interferon-alpha
  • Recombinant Proteins
  • Viral Nonstructural Proteins
  • Deoxycytidine
  • Polyethylene Glycols
  • Ribavirin
  • NS-5 protein, hepatitis C virus
  • peginterferon alfa-2a