Abstract
As biology becomes more quantitative, it appears that the increasing use of mathematics in this area is inevitable. In 1996, Nowak & Bangham (1996, Science 272, 74–79) proposed three mathematical models to explore the relation between antiviral immune responses, virus load, and virus diversity. In this paper we investigate the delay effect in a model which considers the interaction between a replicating virus and host cells. We assume that there is a finite time lag between infection of a cell and the emission of viral particles. Even with the introduction of this delay, the steady states of the model—as suggested by Nowak & Bangham—remain stable. The result also gives a condition for how the parameter values should be chosen when analysing clinical data so that the model remains tenable.
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