Katja C. Wolthers, Hanneke Schuitemaker and Frank Miedema ver the past ten years, many pieces of information have gradually changed the picture of human immunodeficiency virus 1 (HIV-1) pathogenesis. Originally, it was believed that the virus was dormant during clinical latency, despite the well-established effects on immune function and immune activation that occur even before CD4+ T cells are depleted 1. With the development of polymerase chain reaction (PCR)-based amplification techniques and the discovery of high amounts of virus in the lymphoid tissues, it was realized that there might be more virus in the body than was previously thought 2-6. However, the first insight into the magnitude of viral replication dynamics was pro-