ArticlePLoS biology2021
A quantitative model used to compare within-host SARS-CoV-2, MERS-CoV, and SARS-CoV dynamics provides insights into the pathogenesis and treatment of SARS-CoV-2.
Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed.
- Population pharmacokinetic/pharmacodynamic modelling to evaluate favipiravir in combination with lopinavir-ritonavir in patients with COVID-19.British journal of clinical pharmacology · 2026Trial
- Transmission of mutated SARS-CoV-2 variants is favored by relatively prolonged infections due to delayed immunity.bioRxiv : the preprint server for biology · 2026Article
- Spatial Immune Model of Alveolar Lung Infection (SIMALI) Identifies Structural Determinants of Lung Inflammation.Research square · 2026Article
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- Ordinary differential equation models of SARS-CoV-2 replication dynamics and antiviral drug efficacies.Npj viruses · 2026Review
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- Modeling viral shedding and symptom outcomes in oseltamivir-treated experimental influenza infection.PloS one · 2026Article
- Model-informed prediction of antiviral drug combination synergy from sparse data using complementary mechanistic and pharmacodynamic approaches.Frontiers in pharmacology · 2026Article
- Modelling the Variability in Immunity Build-Up and Waning Following RNA-Based Vaccination.Viruses · 2025Article
- Enhancing viral dynamics modeling: reliable initial estimation and validity conditions for quasi-steady state approximation (QSSA).BMC biology · 2025Article
- Modeling Antibody Kinetics Post-mRNA Booster Vaccination and Protection Durations Against SARS-CoV-2 Infection.Journal of medical virology · 2025Article
- Using virtual patient cohorts to uncover immune response differences in cancer and immunosuppressed COVID-19 patients.PLoS computational biology · 2025Article
- Modeling suggests SARS-CoV-2 rebound after nirmatrelvir-ritonavir treatment is driven by target cell preservation coupled with incomplete viral clearance.Journal of virology · 2025Article
- Age- and vaccination status-dependent isolation guidelines based on simulation of SARS-CoV-2 Delta cases in Singapore.Communications medicine · 2025Article
- Modelling and investigating memory immune responses in infectious disease. Application to influenza a virus and sars-cov-2 reinfections.Infectious Disease Modelling · 2025Article
- A modeling study to define guidelines for antigen screening in schools and workplaces to mitigate COVID-19 outbreaks.Communications medicine · 2025Article
- Defining the Critical Requisites for Accurate Simulation of SARS-CoV-2 Viral Dynamics: Patient Characteristics and Data Collection Protocol.Journal of medical virology · 2025Article
- Future Directions for Quantitative Systems Pharmacology.Handbook of experimental pharmacology · 2025Review
- A biomathematical model of SARS-CoV-2 in Syrian hamsters.Scientific reports · 2024Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The scientific community is focused on developing antiviral therapies to mitigate the impacts of the ongoing novel coronavirus disease 2019 (COVID-19) outbreak. This will be facilitated by improved understanding of viral dynamics within infected hosts. Here, using a mathematical model in combination with published viral load data, we compare within-host viral dynamics of SARS-CoV-2 with analogous dynamics of MERS-CoV and SARS-CoV. Our quantitative analyses using a mathematical model revealed that the within-host reproduction number at symptom onset of SARS-CoV-2 was statistically significantly larger than that of MERS-CoV and similar to that of SARS-CoV. In addition, the time from symptom onset to the viral load peak for SARS-CoV-2 infection was shorter than those of MERS-CoV and SARS-CoV. These findings suggest the difficulty of controlling SARS-CoV-2 infection by antivirals. We further used the viral dynamics model to predict the efficacy of potential antiviral drugs that have different modes of action. The efficacy was measured by the reduction in the viral load area under the curve (AUC). Our results indicate that therapies that block de novo infection or virus production are likely to be effective if and only if initiated before the viral load peak (which appears 2-3 days after symptom onset), but therapies that promote cytotoxicity of infected cells are likely to have effects with less sensitivity to the timing of treatment initiation. Furthermore, combining a therapy that promotes cytotoxicity and one that blocks de novo infection or virus production synergistically reduces the AUC with early treatment. Our unique modeling approach provides insights into the pathogenesis of SARS-CoV-2 and may be useful for development of antiviral therapies.
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