ArticleAntiviral therapy2014
Treatment of hepatitis C with an interferon-based lead-in phase: a perspective from mathematical modelling.
Article in Antiviral therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Viral dynamic modelling of Hepatitis C and resistance-associated variants in haemophiliacs.Haemophilia : the official journal of the World Federation of Hemophilia · 2016Trial
- Modelling how responsiveness to interferon improves interferon-free treatment of hepatitis C virus infection.PLoS computational biology · 2018Article
- Modelling the prevalence of hepatitis C virus amongst blood donors in Libya: An investigation of providing a preventive strategy.World journal of virology · 2016Article
- Modeling dynamics of culex pipiens complex populations and assessing abatement strategies for West Nile Virus.PloS one · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe standard of care for HCV genotype 1 is a protease inhibitor (telaprevir or boceprevir) combined with pegylated interferon (PEG-IFN) and ribavirin (RBV). A lead-in phase of PEG-IFN/RBV therapy before addition of the protease inhibitor has been used, with the aim of improving response rates by reducing the development of protease inhibitor resistance. However, whether such a strategy can bring benefit to patients is unclear.
methodsA viral dynamic model was used to compare in silico HCV dynamics in patients treated with a period of PEG-IFN/RBV lead-in therapy followed by the addition of a protease inhibitor versus immediate triple therapy without lead-in.
resultsThe model predicts that both regimens result in a similar end-of-treatment viral load change (viral decline or breakthrough). Thus, the current lead-in strategy may not decrease the rate of viral breakthrough/relapse or increase the rate of sustained virological response. This agrees with available data from clinical trials of several HCV protease inhibitors, such as telaprevir, boceprevir and faldaprevir.
conclusionsThese results suggest that current PEG-IFN/RBV lead-in strategies may not improve treatment outcomes. However, viral kinetics during a period of PEG-IFN/RBV therapy, combined with other factors, such as the IL28B polymorphism and baseline viral load, can identify IFN-sensitive patients and help develop response-guided therapies.
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