Catherine A. A. Beauchemin

TL;DR: A series of mathematical models of increasing complexity, which incorporate target cell limitation and the innate interferon response, are utilized to examine influenza A virus kinetics in the upper respiratory tracts of experimentally infected adults to suggest that antiviral treatments have a large hurdle to overcome in moderating symptoms and limiting infectiousness.

TL;DR: This work explores the symbiotic role of mathematical models and experimental assays in improving the quantitative understanding of influenza infection dynamics, and discusses the challenges in developing better, more comprehensive models for the course of influenza infections within a host or cell culture.

TL;DR: Various agent-based models relevant to host–pathogen systems and their contributions to the authors' understanding of biological processes are reviewed and some limitations and challenges are pointed out.

TL;DR: A simple 2-D cellular automaton (CA) model of a viral infection has been developed and is validated against clinical immunological data for uncomplicated influenza A infections.

TL;DR: It is found that influenza A/Albany/1/98 (H3N2) virions under normal experimental conditions at 37 degrees C rapidly lose infectivity with a half-life of approximately 6.6+/-0.2 h, and that the lifespan of productively infected MDCK cells is approximately 13 h.