The modern era of antiretroviral therapy (ART) for human immunodeficiency virus type 1 (HIV-1) infection began in the mid-1990s with the introduction of 2 new classes of antiretroviral drugs, the protease inhibitors (PIs) and the nonnucleoside reverse-transcriptase inhibitors. Combinations consisting of 1 of these drugs along with 2 nucleoside analogue reverse-transcriptase inhibitors rapidly reduced plasma HIV-1 RNA levels to below the limit of detection of clinical assays [1, 2], leading to predictions that continued treatment for 2–3 years could cure the infection [3]. Although it did not prove curative, combination ART became the mainstay of HIV treatment, allowing durable control of viral replication and reversal or prevention of immunodeficiency [4].

A major reason why ART did not prove curative is the persistence of a latent form of the virus in a small population of resting memory CD4+ T cells [5, 6]. In these cells, the viral genome is stably integrated into host cell DNA, but viral genes are not