摘要：HIV latency remains a major obstacle to viral elimination. The activation rate of latently infected cells may depend on the age of latent infection. In this paper, we develop a model of HIV infection including age-structured latently infected cells. We mathematically analyse the model and use numerical simulations with different activation functions to show that the model can explain the persistence of low-level viremia and the latent reservoir stability in patients on therapy. Sensitivity tests suggest that the model is robust to the changes of most parameters but is sensitive to the relative magnitude of the net generation rate and the long-term activation rate of latently infected cells. To reduce the sensitivity, we extend the model to include homeostatic proliferation of latently infected cells. The new model is robust in reproducing the long-term dynamics of the virus and latently infected cells observed in patients receiving prolonged combination therapy.
