To fully test how a metapopulation structure might affect the predicted dynamics of the model over the entire course of the infection, and to fit it against early and late infection clinical data, would require further processes, such as HIV-specific CTL accumulation, CD4+ T cell loss at the systemic level, or evolution of CTL escape, to be modeled mechanistically or, at least, as external driving factors carefully parameterized from data. Here, CD4 is linked to infection.