Literature DB >> 11948360

Hepatitis C: therapeutic perspectives.

M Cornberg1, H Wedemeyer, M P Manns.   

Abstract

Continuous efforts are vital to develop new treatment strategies to improve sustained response rates, especially for difficult to treat patients infected with the hepatitis C virus. Despite the introduction of ribavirin, more than 50% of the patients do not eliminate the virus with the current standard therapy of interferon-a (IFN) and ribavirin. Options to further enhance response rates include modification of the IFN-dosing schedule with daily dosing of IFN, new IFN such as consensus interferon or modified IFN with longer half-life and more favourable pharmacokinetics such as pegylated IFN (PEG-IFN). Clinical trials with new IFN showed that consensus IFN may improve response rates in unsuccessfully pre-treated patients and patients with HCV-genotype-1. Treatments with PEG-IFN will double response rates achieved with standard IFN monotherapy. The combination of PEG-IFN and ribavirin improves the virological response to more than 50% and even to more than 80% in patients with genotype 2 or 3. By now, standard therapy of chronic hepatitis C has been changed to the combination of PEG-IFN plus ribavirin. Future anti-viral drugs may comprise molecules that directly inhibit HCV proteins and interfere with viral replication. NS3/4A serine protease, ribonucleic acid (RNA) helicase, RNA-dependent RNA polymerase may be potential targets for new drugs. Furthermore antisense oligonucleotides or ribozymes may become new treatment options to inhibit HCV replication. Finally, immunotherapies to enhance HCV-specific immune responses are also attractive strategies to control HCV infection and to prevent chronic liver disease.

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Year:  2001        PMID: 11948360

Source DB:  PubMed          Journal:  Forum (Genova)        ISSN: 1121-8142


  5 in total

1.  Efficient replication of hepatitis C virus genotype 1a RNAs in cell culture.

Authors:  Keril J Blight; Jane A McKeating; Joseph Marcotrigiano; Charles M Rice
Journal:  J Virol       Date:  2003-03       Impact factor: 5.103

2.  Antisense oligonucleotide inhibition of hepatitis C virus genotype 4 replication in HepG2 cells.

Authors:  Mostafa K el-Awady; Noha G Badr el-Din; Wael T el-Garf; Samar S Youssef; Moataza H Omran; Jasmin el-Abd; Said A Goueli
Journal:  Cancer Cell Int       Date:  2006-06-27       Impact factor: 5.722

3.  JAK-inhibitor and type I interferon ability to produce favorable clinical outcomes in COVID-19 patients: a systematic review and meta-analysis.

Authors:  Lucas Walz; Avi J Cohen; Andre P Rebaza; James Vanchieri; Martin D Slade; Charles S Dela Cruz; Lokesh Sharma
Journal:  BMC Infect Dis       Date:  2021-01-11       Impact factor: 3.090

4.  Selected replicon variants with low-level in vitro resistance to the hepatitis C virus NS5B polymerase inhibitor PSI-6130 lack cross-resistance with R1479.

Authors:  Samir Ali; Vincent Leveque; Sophie Le Pogam; Han Ma; Friederike Philipp; Nicole Inocencio; Mark Smith; Andre Alker; Hyunsoon Kang; Isabel Najera; Klaus Klumpp; Julian Symons; Nick Cammack; Wen-Rong Jiang
Journal:  Antimicrob Agents Chemother       Date:  2008-10-06       Impact factor: 5.191

5.  Characterization of the antiviral effects of interferon-alpha against a SARS-like coronoavirus infection in vitro.

Authors:  Joanna Zorzitto; Carole L Galligan; Joanna J M Ueng; Eleanor N Fish
Journal:  Cell Res       Date:  2006-02       Impact factor: 25.617

  5 in total

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