Modelling dynamics of the type I interferon response to in vitro viral infection

被引：40

作者：

Howat, Tom J.

Barreca, Cristina

O'Hare, Peter

Gog, Julia R.

Grenfell, Bryan T.

机构：

[1] Univ Cambridge, Dept Zool, Cambridge CB2 3EJ, England

[2] Marie Curie Res Inst, Oxted RH8 0TL, Surrey, England

[3] Penn State Univ, Dept Biol, State Coll, Ctr Infect Dis Dynam, University Pk, PA 16802 USA

[4] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA

来源：

JOURNAL OF THE ROYAL SOCIETY INTERFACE | 2006年 / 3卷 / 10期

关键词：

innate immunity; viral infection; cytokines; interferon; stochastic model; dose dependence;

D O I：

10.1098/rsif.2006.0136

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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 during in vitro infection of Madin-Darby bovine kidney cell monolayers by Herpes simplex virus 1. The dose dependence of infection progression, subsequent monolayer destruction and IFN-beta production are investigated. Implications for in vivo infections, in particular the priming of susceptible cells by IFN-beta during infection, are considered.

引用

页码：699 / 709

页数：11

共 43 条

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