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Related Concept Videos

Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Inhibitors of Viral Protein Synthesis01:30

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Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
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Retroviruses

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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Published on: September 25, 2019

Antiviral therapy: chronic hepatitis C.

E Jenny Heathcote1

  • 1University of Toronto, Toronto, ON, Canada. jenny.heathcote@utoronto.ca

Journal of Viral Hepatitis
|November 21, 2007
PubMed
Summary

Pegylated interferon and ribavirin are standard for chronic hepatitis C, with treatment durations varying by genotype. Adjusting therapy duration based on early hepatitis C virus (HCV) clearance or slow response can optimize sustained virologic response (SVR) rates.

Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • Pegylated interferon (IFN) with ribavirin is the established treatment for chronic hepatitis C.
  • Treatment durations vary: 48 weeks for genotype 1 and 24 weeks for genotypes 2/3.
  • Current strategies aim to optimize treatment efficacy and duration.

Purpose of the Study:

  • To review current treatment strategies for chronic hepatitis C.
  • To explore modifications in treatment duration based on viral kinetics.
  • To discuss emerging therapies and future directions in hepatitis C treatment.

Main Methods:

  • Review of existing literature on pegylated interferon and ribavirin therapy for chronic hepatitis C.
  • Analysis of treatment response based on hepatitis C virus (HCV) genotype and viral load.

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  • Examination of strategies for treatment shortening or prolongation to improve sustained virologic response (SVR).

    • Main Results:

    • Treatment shortening to 12-24 weeks is feasible for certain genotypes with early HCV clearance, maintaining SVR.
    • Prolonging treatment to 72 weeks for 'slow responders' improves SVR by reducing relapse.
    • Over 50% of patients remain relapsers or nonresponders, indicating a need for improved therapies.

    Conclusions:

    • Optimizing treatment duration based on early viral response can enhance SVR rates in chronic hepatitis C.
    • Retreatment may be beneficial for nonresponders, depending on prior treatment adequacy.
    • New antiviral agents and immunomodulatory therapies are under development to improve efficacy and tolerability.