Introduction
The ongoing human immunodeficiency virus (HIV) pandemic continues unabated with over 37 million people infected in spite of the availability of a large number of antiretroviral drugs (1). The current combination antiretroviral therapy (ART) while highly effective at controlling viral replication, is however unable to eliminate the virus, which readily rebounds upon ART cessation. Therefore, the development of a protective vaccine remains a priority, though this task is complicated by a relatively poor understanding of immune correlates of protection at this time. In addition, the persistence of HIV infection in spite of potent combinations of drugs also remains to be fully elucidated. Even more puzzling, the ongoing vigorous but inadequate antiviral immune response both during and post ART remains unable to contain chronic virus replication. Most active HIV replication occurs in CD4 T cells in secondary lymphoid organs (2, 3), and recent data also highlights these sites as important reservoirs of latent infection during ART (4, 5). Moreover, these reservoirs are seeded early postinfection (6), and early ART may decrease the size of cells harboring HIV DNA (7, 8), although an exact temporal relation between seeding magnitude of various anatomical reservoirs and specific cell lineages remains to be fully elucidated for both HIV and SIV. During the course of infection, virus has been shown to remain in the germinal center (GC) of hyperplastic follicles, while the architecture of the lymph node experiences gradual remodeling (2, 9).