Lopacinski2021 - Coxsackievirus B3 (CVB3) complete kinetics ODE model
Ontology highlight
ABSTRACT:
SUBMITTER: 
Kevin Janes
PROVIDER: MODEL2110250001 | BioModels | 2021-10-26
REPOSITORIES: BioModels
Publications
Modeling the complete kinetics of coxsackievirus B3 reveals human determinants of host-cell feedback.
Lopacinski Aaron B AB Sweatt Andrew J AJ Smolko Christian M CM Gray-Gaillard Elise E Borgman Cheryl A CA Shah Millie M Janes Kevin A KA
Cell systems 20210318 4
Complete kinetic models are pervasive in chemistry but lacking in biological systems. We encoded the complete kinetics of infection for coxsackievirus B3 (CVB3), a compact and fast-acting RNA virus. The model consists of separable, detailed modules describing viral binding-delivery, translation-replication, and encapsidation. Specific module activities are dampened by the type I interferon response to viral double-stranded RNAs (dsRNAs), which is itself disrupted by viral proteinases. The experi ...[more]
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Project description:This ordinary differential equation model is described in the following article:
"Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host"
G. Michael Lavigne, Hayley Russell, Barbara Sherry and Ruian Ke
DOI: 10.1098/rspb.2020.3002
Comment:
This model is based on the ordinary differential equations of the non-spatial model of well-mixed viral infection stated in the manuscript (Eq. 2.1 in the article).
Abstract:
The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.
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