ArticlePLoS computational biology2013
Multiscale modeling of influenza A virus infection supports the development of direct-acting antivirals.
Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 79 citations in OpenAlex.
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- Modification of surface glycan by expression of beta-1,4-N-acetyl-galactosaminyltransferase (B4GALNT2) confers resistance to multiple viruses infection in chicken fibroblast cell.Frontiers in veterinary science · 2023Article
- Mathematical modeling of plus-strand RNA virus replication to identify broad-spectrum antiviral treatment strategies.bioRxiv : the preprint server for biology · 2022Article
- Mathematical modelling of SARS-CoV-2 infection of human and animal host cells reveals differences in the infection rates and delays in viral particle production by infected cells.Journal of theoretical biology · 2021Article
- Advancing therapies for viral infections using mechanistic computational models of the dynamic interplay between the virus and host immune response.Current opinion in virology · 2021Review
- Multiscale model of defective interfering particle replication for influenza A virus infection in animal cell culture.PLoS computational biology · 2021Article
- Quantification of Ebola virus replication kinetics in vitro.PLoS computational biology · 2020Article
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- A Coupled Mathematical Model of the Intracellular Replication of Dengue Virus and the Host Cell Immune Response to Infection.Frontiers in microbiology · 2020Article
- Model-based analysis of influenza A virus replication in genetically engineered cell lines elucidates the impact of host cell factors on key kinetic parameters of virus growth.PLoS computational biology · 2019Article
- Multiscale modeling of influenza A virus replication in cell cultures predicts infection dynamics for highly different infection conditions.PLoS computational biology · 2019Article
- Production of Defective Interfering Particles of Influenza A Virus in Parallel Continuous Cultures at Two Residence Times-Insights From qPCR Measurements and Viral Dynamics Modeling.Frontiers in bioengineering and biotechnology · 2019Article
- Cell culture-based production of defective interfering particles for influenza antiviral therapy.Applied microbiology and biotechnology · 2018Article
- Investigating Different Mechanisms of Action in Combination Therapy for Influenza.Frontiers in pharmacology · 2018Article
- Mathematical Analysis of Viral Replication Dynamics and Antiviral Treatment Strategies: From Basic Models to Age-Based Multi-Scale Modeling.Frontiers in microbiology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A viruses are respiratory pathogens that cause seasonal epidemics with up to 500,000 deaths each year. Yet there are currently only two classes of antivirals licensed for treatment and drug-resistant strains are on the rise. A major challenge for the discovery of new anti-influenza agents is the identification of drug targets that efficiently interfere with viral replication. To support this step, we developed a multiscale model of influenza A virus infection which comprises both the intracellular level where the virus synthesizes its proteins, replicates its genome, and assembles new virions and the extracellular level where it spreads to new host cells. This integrated modeling approach recapitulates a wide range of experimental data across both scales including the time course of all three viral RNA species inside an infected cell and the infection dynamics in a cell population. It also allowed us to systematically study how interfering with specific steps of the viral life cycle affects virus production. We find that inhibitors of viral transcription, replication, protein synthesis, nuclear export, and assembly/release are most effective in decreasing virus titers whereas targeting virus entry primarily delays infection. In addition, our results suggest that for some antivirals therapy success strongly depends on the lifespan of infected cells and, thus, on the dynamics of virus-induced apoptosis or the host's immune response. Hence, the proposed model provides a systems-level understanding of influenza A virus infection and therapy as well as an ideal platform to include further levels of complexity toward a comprehensive description of infectious diseases.
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