(A) A diagram of the mathematical model. HIV infection is assumed to be restricted to the dividing subsets, as are virion production from cells containing (replication-competent) integrated HIV DNA (
and
). The majority (99.9%) of pVL production was assumed to be non-infectious VNI
[33], while 50% of integration events were replication incompetent. Activation of resting cells β, and rates of proliferation λ, are dependent on pVL in a Michaelis–Menten manner, e.g.
. Infection of target cells followed a similar pattern but was dependent only on the infectious virus component
. (B) Contributions to total pVL (solid) from directly infected (dashed) and clonally expanded infected (dash-dot) memory CD4+T cells from the start of ART commenced at CHI. (C) pVL rebound after cessation of 6 years of ART commenced at CHI. The solution to the initial fitting procedure with bounds on rebound time in red and other fitted solutions from multiple nearby parameter sets in grey.