Abstract
The new field of viral dynamics, based on within-host modeling of viral infections, began with models of human immunodeficiency virus (HIV), but now includes many viral infections. Here we review developments in HIV modeling, emphasizing quantitative findings about HIV biology uncovered by studying acute infection, the response to drug therapy and the rate of generation of HIV variants that escape immune responses. We show how modeling has revealed many dynamical features of HIV infection and how it may provide insight into the ultimate cure for this infection.
Highlights
The new field of viral dynamics, based on within-host modeling of viral infections, began with models of human immunodeficiency virus (HIV), but includes many viral infections
Some modelers have suggested other explanations for this second phase, such as the decline being driven by cytotoxic T lymphocytes (CTLs), which slows as the CTL response declines [27], or that infected cells have an age-dependent transactivation rate, which slows the generation of virus-producing cells [28]
The basic idea, which we discuss in terms of cellmediated responses, is that cells infected by wild-type virus should be susceptible to both viral cytopathic effects and immune-mediated killing, say by CTL responses, whereas a ‘CTL escape variant’ would only be susceptible to viral cytopathic effects
Summary
The new field of viral dynamics, based on within-host modeling of viral infections, began with models of human immunodeficiency virus (HIV), but includes many viral infections. Comparing the first-phase decay rates of various drug regimens allows one to compare their relative effectiveness [22] and using the most potent regimens that approach 100% effectiveness has led to the conclusion that productively infected cells live about one day after they start producing virus [23].
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