Purpose of review: To provide a summary of the contributions of mathematical modeling to understanding of HIV persistence during antiretroviral therapy.
Recent findings: Although HIV persistence during therapy could be caused by continual viral replication or slow-decaying latent infection, most evidence points toward the latter mechanism. The latent reservoir is maintained by a balance of cell death, proliferation, and reactivation, and new methods to estimate the relative contributions of these rates use a wide range of experimental data. This has led to new quantitative predictions about the potential benefit of therapies such as latency-reversing agents or antiproliferative drugs.
Summary: Results of these mathematical modeling studies can be used to design and interpret future trials of new therapies targeting HIV persistence.