Skip Navigation


JAC Advance Access originally published online on September 18, 2009
Journal of Antimicrobial Chemotherapy 2009 64(5):945-948; doi:10.1093/jac/dkp328
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
64/5/945    most recent
dkp328v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Dryer, P. D.
Right arrow Articles by Blackard, J. T.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dryer, P. D.
Right arrow Articles by Blackard, J. T.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Screening for hepatitis C virus non-nucleotide resistance mutations in treatment-naive women

Peter D. Dryer1, Berkeley N. Limketkai1, Christina M. Martin1, Gang Ma1, Kenneth E. Sherman1, Lynn E. Taylor2, Kenneth H. Mayer2, Denise J. Jamieson3 and Jason T. Blackard1,*

1 Division of Digestive Diseases, University of Cincinnati College of Medicine, Cincinnati, OH, USA 2 Miriam Hospital and Department of Medicine, Brown University, Providence, RI, USA 3 Division of Reproductive Health, Centers for Disease Control and Prevention, Atlanta, GA, USA

Received 29 June 2009; returned 19 July 2009; revised 8 August 2009; accepted 12 August 2009


* Corresponding author. Tel: +1-513-558-4389; Fax: +1-513-558-1744; E-mail: jason.blackard{at}uc.edu

Objectives: Hepatitis C virus (HCV) non-nucleoside inhibitors (NNIs) target the viral RNA-dependent RNA polymerase encoded by the NS5B gene. Several NNIs share a similar allosteric binding site, and their antiviral efficacy is attenuated by a cysteine-to-tyrosine mutation at amino acid 316 (C316Y). In the current study, we assessed NS5B resistance mutations in treatment-naive individuals from a prospective natural history study of viral infections in women.

Methods: Partial NS5B sequences from HCV-positive women were amplified by RT–PCR. Additionally, subcloning was performed to evaluate intrapatient variability in selected samples.

Results: HCV NS5B genotypes were 45 genotype 1a (57.0%), 11 genotype 1b (13.9%), 5 genotype 2a (6.3%), 3 genotype 2b (3.8%), 9 genotype 3a (11.4%) and 6 genotype 4a (7.6%). One HCV genotype 1a-infected patient was found to have the C316Y mutation (1.3%). Clonal analysis further revealed that all NS5B sequences from this individual—representing three serum samples collected 4 years apart—contained the C316Y mutation. In contrast, the S282T resistance mutation was not found in any samples.

Conclusions: The C316Y polymerase resistance mutation was found in 1.3% of samples from HCV-infected women. The presence of this mutation over time suggests significant replicative fitness of this variant and has implications for development of new specifically targeted antiviral therapies against HCV (STAT-C) targeting this region.

Keywords: HCV , NS5B , C316Y


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.