447. Mutation May Be Important in Second Generation DAA Treatment Failures
Session: Poster Abstract Session: Hepatitis C
Thursday, October 27, 2016
Room: Poster Hall
  • IDSA 2016 hepC abs poster 9-23-16 draft 3_Final.pdf (334.5 kB)
  • Background:

    The use of DAAs has significantly improved treatment outcomes in patients with chronic HCV. The data on DAA treatment failure is limited. Resistance associated variants (RAVs) seem to play an important role.  We analyzed treatment outcomes and causes of DAAs failure in NJ VA patients over a period of 1.5 years.


    We performed a retrospective health record review of all HCV patients treated between 9/24/14 and 3/4/16. HCV genotypes (GT), the presence of cirrhosis and HIV, DAA type, length of therapy, and RAVs post treatment were evaluated in the treatment failure (TF) group. TF was defined as an inability to achieve the sustained virological response at week 12 post therapy (SVR12).


    238 HCV patients were treated in the outlined period. The treatment success rate was 89.9%. It was 93.4 %( 214/229) when adjusted for the number of patients who fully completed therapy. The failure rate in the latter group was 6.6%.  The TF group had 1 patient with HIV; 10 with cirrhosis, 7 with GT 1a, 2-GT 1b, 4-GT 2b, and 2-GT 3a.  

    8/9 patients with GT 1 received Ledipasvir/Sofosbuvir (LDV/SOF) +/- Ribavirin (RBV) for 12 weeks, 1/9 -Paritaprevir/ritonavir/ombitasvir plus dasabuvir (PrOD) + RBV for 12 weeks. GT 2b patients were treated with SOF/RBV for 12 weeks.  GT 3a were on LDV/SOF +RBV or SOF/RBV for 24 weeks.

    Resistance panel was available for 9 patients.

    GT 1 patients had Q30H/Q80K, Q30H/Y93H, Q30R/Q80K, Q30E/Q80K, and Q30E/S556G RAVs. The patient on PrOD had M28T, M141 M/T, E446 E/K, Q80K, D168 E/Y, and Y93H RAVs.

    1 in 4 GT2b patients had available resistance report with L159F RAV.

    Both patients with GT3a had no SOF or Daclatasvir RAVs found.



    The HCV treatment failure rate in patients who fully completed therapy at the NJ VA over 1.5 years was 6.6% and 3% for those with detected RAVs. All GT1 patients with the available resistance analysis had NS5a RAVs. One patient with GT2b had NS5b RAV. The data on GT3a was incomplete since the full resistance panel was not performed. The information on pre-treatment RAVs was not available making it impossible to determine whether the mutations were natural or emerged on treatment. Analysis of available data indicates that the presence of RAVs might be the major cause of treatment failure among HCV patients treated with DAAs in NJ VA.

    Glen Abergel, MD1, Robert H K Eng, MD2, Sandra Kaminski, MS, PA-C2 and Alexandra Sonyey, MD3, (1)Infectious Diseases, Rutgers University, Newark, NJ, (2)Infectious Disease, VA New Jersey Healthcare System, East Orange, NJ, (3)Infectious Diseases, VA New Jersey Healthcare System, East Orange, NJ


    G. Abergel, None

    R. H. K. Eng, None

    S. Kaminski, None

    A. Sonyey, None

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