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The conundrum of relapse in STAT-C therapy: does HCV play the Red Queen or Rip Van Winkle?

Robert Ralston1, Ira Jacobson, Margaret Scull

  • 1Laboratory of Virology and Infectious Disease and Center for the Study of Hepatitis C, The Rockefeller University, New York, NY, USA. ralstonr@missouri.edu

Seminars in Liver Disease
|December 23, 2011
PubMed

Insights

New hepatitis C treatments effectively lower viral load, but some patients relapse. This suggests the hepatitis C virus (HCV) may persist in forms resistant to current antiviral therapies.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Direct-acting antivirals (DAAs) combined with pegylated interferon and ribavirin (PEG-IFN/RBV) have improved chronic hepatitis C treatment outcomes.
  • Sustained virologic response is common, but a subset of patients relapse after treatment completion despite undetectable viral loads during therapy.

Purpose of the Study:

  • To investigate the molecular mechanisms of hepatitis C virus (HCV) persistence.
  • To understand the clinical virology of relapse in patients treated with DAAs and PEG-IFN/RBV.

Main Methods:

  • Review of HCV molecular biology and replication strategies.
  • Analysis of clinical data on patient relapse following antiviral therapy.

Main Results:

  • HCV may persist in forms resistant to eradication by current antiviral regimens.
  • Relapse suggests the virus can survive extensive antiviral pressure and re-emerge post-treatment.

Conclusions:

  • The persistence of HCV in refractory forms presents a challenge to achieving a complete cure.
  • Further research into viral survival mechanisms is crucial for developing strategies to prevent relapse.

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