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Treatment with integrase inhibitor suggests a new interpretation of HIV RNA decay curves that reveals a subset of cells with slow integration
Fig 2
Schematics of the models.
(A) The standard model with pre- and post-integration phases of infection. We follow two types of target cells that after infection will be short-lived, 
, or long-lived, 
. Target cells, 
, are infected by infectious virus, Vi, at rate 
. The infection can be blocked by the activity of RTIs with effectiveness η. These infected cells, I1, are lost at rate δ1, or can undergo provirus integration at rate k and become productively infected cells I2. InSTIs block integration with efficacy ω. Cells with integrated provirus, I2, are lost at rate δ2. Virions are produced by these cells at rate p per cell and are cleared from the circulation at rate c per virion. Protease inhibitors block the production of infectious virus VIi, and lead to production of non-infectious virus VIni, with efficacy ε. The subscripts I and M are used to distinguish virions produced by short-lived and long-lived infected cells, respectively. The dynamics of long-lived cells are similar, but possibly with different rates as indicated. (B) The slow and rapid integration (SRI) model. The SRI model proposes that both short-lived cells with fast integration (I1) and long-lived cells with slow integration (M1) generate productively infected cells that die quickly (I2) (i.e. δ2 = δM2).
doi: https://doi.org/10.1371/journal.ppat.1006478.g002