Similarly, distribution of the proportion of patients experiencing viral rebound after therapy cessation was addressed (figure 3B).
Even more interesting is to notice the swift viral rebound at therapy discontinuation in the early and late cases.
However no tested purging strategy has proven capable of eliminating the infection completely or preventing viral rebound if therapy is stopped.
The results obtained from this modeling study indicate that the response of tumors capable of dedifferentiating is qualitatively different from a scenario in which treatment cannot completely eradicate the bulk of tumor cells and the remaining cells lead to a rebound post-therapy.
Sustained treatment interruption may pose a greater risk of virologic rebound on NNRTI therapy than the same number of interspersed missed doses at low-to-moderate adherence.
In addition, after discontinuing hyperosmolar therapy, rebound effects may occur [ 60, 63- 65].
Foo et al. (this issue) model tumor rebound growth following therapy and find that tumor diversity predicts early relapse when mutation rates are high.
In contrast, the addition of an entry inhibitor (anti-CD81 mAb or erlotinib) at the time of simeprevir withdrawal allowed to further decrease the viral load, indicating that entry inhibitors limit viral rebound from DAA therapy.
Figure 2 summarizes data of virological rebound (averages) after therapy interruption at different time points (4, 8 and 24 weeks) for very early and late patients for both clinical (empty boxes) and simulation data (filled boxes).
