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Both effects are important aims of therapy. A number of models have been proposed for both processes, and for joint descriptions of viral and T-cell responses, although most have only been applied to adult data, and very few have also incorporated drug PK. Various approaches have been taken to quantifying and modelling viral suppression in HIV-infected children on ART. The simplest pharmacodynamic studies assess correlations between measures of drug exposure (AUC, peak or trough plasma concentration) and viral suppression this website (typically time to undetectable viral load, or reduction in viral load by a specified time point). Studies of this kind were comprehensively reviewed in 2011 by Neely and Rakhmanina [155]. More advanced mechanistic models of the virological activity of ART predict a biphasic decay in viral load [156], and models Dabrafenib chemical structure of this kind have been successfully fitted in a mixed-effects framework to data from infants (Ritonavir and Brazilian children to construct predictive models of long-term CD4 counts, given characteristics measurable at ART initiation (again including age and viral load) [159]. Models of this type have great potential for informing guidelines for ART initiation and individual patient management, as these children increasingly survive into adulthood and long-term immunological health becomes a more pressing question. Finally, the same simple exponential model was also used to demonstrate contrasts between recovery in children and in adults, which are likely to be due to the importance of the thymus and the na?ve T-cell pool to children's T-cell dynamics [160]. A number of joint models of viral and T-cell dynamics in HIV have been developed and applied in a mixed-effects framework, many of which use adult data. While adult models provide an important starting point, epidemiological evidence suggests that both virological and immunological responses to HIV infection and ART are different in adults and children [161].