Analysis of hepatitis C NS5A resistance associated polymorphisms using ultra deep single molecule real time (SMRT) sequencing

Antiviral Res. 2016 Feb:126:81-9. doi: 10.1016/j.antiviral.2015.12.005. Epub 2015 Dec 19.

Abstract

Development of Hepatitis C virus (HCV) resistance against direct-acting antivirals (DAAs), including NS5A inhibitors, is an obstacle to successful treatment of HCV when DAAs are used in sub-optimal combinations. Furthermore, it has been shown that baseline (pre-existing) resistance against DAAs is present in treatment naïve-patients and this will potentially complicate future treatment strategies in different HCV genotypes (GTs). Thus the aim was to detect low levels of NS5A resistant associated variants (RAVs) in a limited sample set of treatment-naïve patients of HCV GT1a and 3a, since such polymorphisms can display in vitro resistance as high as 60000 fold. Ultra-deep single molecule real time (SMRT) sequencing with the Pacific Biosciences (PacBio) RSII instrument was used to detect these RAVs. The SMRT sequencing was conducted on ten samples; three of them positive with Sanger sequencing (GT1a Q30H and Y93N, and GT3a Y93H), five GT1a samples, and two GT3a non-positive samples. The same methods were applied to the HCV GT1a H77-plasmid in a dilution series, in order to determine the error rates of replication, which in turn was used to determine the limit of detection (LOD), as defined by mean + 3SD, of minority variants down to 0.24%. We found important baseline NS5A RAVs at levels between 0.24 and 0.5%, which could potentially have clinical relevance. This new method with low level detection of baseline RAVs could be useful in predicting the most cost-efficient combination of DAA treatment, and reduce the treatment duration for an HCV infected individual.

Keywords: Deep sequencing; Hepatitis C virus; NS5A; Pacific biosciences; RAV; Resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology*
  • Base Sequence
  • Drug Resistance, Viral / drug effects
  • Drug Resistance, Viral / genetics*
  • Hepacivirus / drug effects
  • Hepacivirus / genetics*
  • Hepatitis C / drug therapy
  • Hepatitis C / genetics*
  • Hepatitis C / therapy
  • High-Throughput Nucleotide Sequencing / methods*
  • Humans
  • Mutation
  • Polymerase Chain Reaction
  • Polymorphism, Genetic
  • Sequence Analysis, DNA
  • Viral Nonstructural Proteins / genetics*
  • Virus Replication / genetics

Substances

  • Antiviral Agents
  • Viral Nonstructural Proteins
  • NS-5 protein, hepatitis C virus