Editorial
Copyright ©2007 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 21, 2007; 13(43): 5673-5681
Published online Nov 21, 2007. doi: 10.3748/wjg.v13.i43.5673
Specifically targeted antiviral therapy for hepatitis C virus
Anna Parfieniuk, Jerzy Jaroszewicz, Robert Flisiak
Anna Parfieniuk, Jerzy Jaroszewicz, Robert Flisiak, Department of Infectious Diseases, Medical University of Bialystok, Zurawia St 14, Bialystok 15540, Poland
Author contributions: All authors contributed equally to the work.
Correspondence to: Robert Flisiak, Department of Infectious Diseases, Medical University of Bialystok, Zurawia St 14, Bialystok 15540, Poland. flisiakr@priv.onet.pl
Telephone: +48-85-7416921 Fax: +48-85-7416921
Received: June 19, 2007
Revised: July 29, 2007
Accepted: September 13, 2007
Published online: November 21, 2007
Abstract

Hepatitis C virus (HCV) infection affects 180 million people worldwide with the predominant prevalence being infection with genotype 1, followed by genotypes 2 and 3. Standard anti-HCV therapy currently aims to enhance natural immune responses to the virus, whereas new therapeutic concepts directly target HCV RNA and viral enzymes or influence host-virus interactions. Novel treatment options now in development are focused on inhibitors of HCV-specific enzymes, NS3 protease and NS5B polymerase. These agents acting in concert represent the concept of specifically targeted antiviral therapy for HCV (STAT-C). STAT-C is an attractive strategy in which the main goal is to increase the effectiveness of antiviral responses across all genotypes, with shorter treatment duration and better tolerability. However, the emergence of resistant mutations that limit the use of these compounds in monotherapy complicates the regimens. Thus, a predictable scenario for HCV treatment in the future will be combinations of drugs with distinct mechanisms of action. For now, it seems that interferon will remain a fundamental component of any new anti-HCV therapeutic regimens in the near future; therefore, there is pressure to develop forms of interferon that are more effective, less toxic, and more convenient than pegylated interferon.

Keywords: Hepatitis C virus; Chronic hepatitis C; Polymerase inhibitors; Protease inhibitors; Cyclophilin B inhibitors