Modelling dynamics of the type I interferon response toin vitroviral infection

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Abstract
Innate immunity is crucial in the early stages of resistance to novel viral infection. The family of cytokines known as the interferons (IFNs) forms an essential component of this system: they are responsible for signalling that an infection is underway and for promoting an antiviral response in susceptible cells. We construct a spatial stochastic model, parameterized by experimental data and informed by analytic approximation, to capture the dynamics of virus–IFN interaction duringin vitroinfection of Madin–Darby bovine kidney cell monolayers by Herpes simplex virus 1. The dose dependence of infection progression, subsequent monolayer destruction and IFN-β production are investigated. Implications forin vivoinfections, in particular the priming of susceptible cells by IFN-β during infection, are considered.