ArticleCPT: pharmacometrics & systems pharmacology2015
Modeling Suggests a Mechanism of Synergy Between Hepatitis C Virus Entry Inhibitors and Drugs of Other Classes.
Article in CPT: pharmacometrics & systems pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- How robust are estimates of key parameters in standard viral dynamic models?PLoS computational biology · 2024Article
- Global asymptotic stability of a delay differential equation model for SARS-CoV-2 virus infection mediated by ACE2 receptor protein.Applied mathematics letters · 2023Article
- Mechanistic Models of COVID-19: Insights into Disease Progression, Vaccines, and Therapeutics.International journal of antimicrobial agents · 2022Review
- Life cycle process dependencies of positive-sense RNA viruses suggest strategies for inhibiting productive cellular infection.Journal of the Royal Society, Interface · 2021Article
- Targeting TMPRSS2 and Cathepsin B/L together may be synergistic against SARS-CoV-2 infection.PLoS computational biology · 2020Article
- Interferon at the cellular, individual, and population level in hepatitis C virus infection: Its role in the interferon-free treatment era.Immunological reviews · 2018Review
- Modelling how responsiveness to interferon improves interferon-free treatment of hepatitis C virus infection.PLoS computational biology · 2018Article
- Hepatitis C virus cell entry: a target for novel antiviral strategies to address limitations of direct acting antivirals.Hepatology international · 2016Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) entry inhibitors (EIs) act synergistically with drugs targeting other stages of the HCV lifecycle. The origin of this synergy remains unknown. Here, we argue that the synergy may arise from the complementary activities of the drugs across cell subpopulations expressing different levels of HCV entry receptors. We employ mathematical modeling of viral kinetics in vitro, where cells with a distribution of entry receptor expression levels are exposed to HCV with or without drugs. The drugs act independently in each cell, as expected in the absence of underlying interactions. Yet, at the cell population level our model predicts that the drugs exhibit synergy. EIs effectively block infection of cells with low receptor levels. With high receptor levels, where EIs are compromised, other drugs are potent. This novel mechanism of synergy, arising at the cell population level may facilitate interpretation of drug activity and treatment optimization.
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Registered trials
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