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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2015 Jun 30;12(8):437–445. doi: 10.1038/nrgastro.2015.97

Figure 2.

Figure 2

Comparison of the standard viral dynamic model and a multiscale model. a) In the standard model target cells, T, are produced at rate s (not shown) and become infected with rate constant β by interacting with virus and die at per capita rate d. Infected cells, I, produce virus at rate p per cell and die at per capita rate δ. Finally, virus, V, in addition to being produced is cleared at rate c per virion. Treatment reduces the average number of virions produced by an infected cell from p to p(1 − ε). The effectiveness of a drug, ε, represents a global measure of antiviral effectiveness that does not distinguish between the stages of intracellular viral replication, assembly and release that are blocked by treatment. b) The multiscale model accounts for intracellular processes involving HCV RNA (vRNA), R, that is, production, degradation and assembly and secretion with rate parameters α, μ, and ρ, respectively. The vRNA level within an infected cell (dashed circle) is assumed to increase with time since the first infection, that is, the age of an infected cell, a, and ultimately reaches a steady state. Treatment (parameters in red) can block vRNA production with effectiveness ε±, and/or virion assembly and secretion with effectiveness εs, and/or enhance the degradation rate of vRNA by a factor κ. Reproduced with permission from Guedj et al. Proc. Natl. Acad. Sci. USA 110: 3991–3996 (2013).