ArticlePloS one2019
Uncovering critical properties of the human respiratory syncytial virus by combining in vitro assays and in silico analyses.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- In Vitro Analysis and Dynamic Modeling of SARS-CoV-2 Infection Inhibition by Sigma-1 Receptor Antagonist PB28.Bulletin of mathematical biology · 2026Article
- Sensitivity of RSV detection by PCR in respiratory samples is not reduced by a 24 h delay from sampling to testing with storage at room temperature.Molecular medicine (Cambridge, Mass.) · 2025Article
- Intracellular and extracellular dynamics of herpes simplex virus 1 DNA and infectious particles in epithelial and neuronal cells.bioRxiv : the preprint server for biology · 2025Article
- Analyzing Differences in Viral Dynamics Between Vaccinated and Unvaccinated RSV Patients.Epidemiologia (Basel, Switzerland) · 2025Article
- Practical parameter identifiability and handling of censored data with Bayesian inference in mathematical tumour models.NPJ systems biology and applications · 2024Article
- Potentiality of bioactive compounds as inhibitor of M protein and F protein function of human respiratory syncytial virus.In silico pharmacology · 2024Article
- Efficient assays to quantify the life history traits of algal viruses.Applied and environmental microbiology · 2023Article
- The effect of random virus failure following cell entry on infection outcome and the success of antiviral therapy.Scientific reports · 2023Article
- 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
- Dynamical Differences in Respiratory Syncytial Virus.Bulletin of mathematical biology · 2021Article
- Time to revisit the endpoint dilution assay and to replace the TCID50 as a measure of a virus sample's infection concentration.PLoS computational biology · 2021Article
- Quantifying dose-, strain-, and tissue-specific kinetics of parainfluenza virus infection.PLoS computational biology · 2021Article
- Energy Requirements for Loss of Viral Infectivity.Food and environmental virology · 2020Article
- Quantification of Ebola virus replication kinetics in vitro.PLoS computational biology · 2020Article
- Article
- Mathematical modelling identifies the role of adaptive immunity as a key controller of respiratory syncytial virus in cotton rats.Journal of the Royal Society, Interface · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many aspects of the respiratory syncytial virus (RSV) are still poorly understood. Yet these knowledge gaps have had and could continue to have adverse, unintended consequences for the efficacy and safety of antivirals and vaccines developed against RSV. Mathematical modelling was used to test and evaluate hypotheses about the rate of loss of RSV infectivity and the mechanisms and kinetics of RSV infection spread in SIAT cells in vitro. While the rate of loss of RSV integrity, as measured via qRT-PCR, is well-described by an exponential decay, the latter mechanism failed to describe the rate at which RSV A Long loses infectivity over time in vitro based on the data presented herein. This is unusual given that other viruses (HIV, HCV, influenza) have been shown to lose their infectivity exponentially in vitro, and indeed an exponential rate of loss of infectivity is always assumed in mathematical modelling and experimental analyses. The infectivity profile of RSV in HEp-2 and SIAT cells remained consistent over the course of an RSV infection, over time and a large range of infectivity. However, SIAT cells were found to be ∼ 100× less sensitive to RSV infection than HEp-2 cells. In particular, we found that RSV spreads inefficiently in SIAT cells, in a manner we show is consistent with the establishment of infection resistance in uninfected cells. SIAT cells are a good in vitro model in which to study RSV in vivo dissemination, yielding similar infection timescales. However, the higher sensitivity of HEp-2 cells to RSV together with its RSV infectivity profile being similar to that of SIAT cells, makes HEp-2 cells more suitable for quantifying RSV infectivity over the course of in vitro RSV infections in SIAT cells. Our findings highlight the importance and urgency of resolving the mechanisms at play in the dissemination of RSV infections in vitro, and the processes by which this infectivity is lost.
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