Suppression of the immune system was first documented 88 years ago by Clement von Pirquet (4) who observed that the tuberculin skin test of immune individuals was depressed during the course of acute MV infection from just prior to the rash until 1–2 months or more following its appearance. Although transiently depressed, the degree of immune suppression was sufficiently severe that prior to the discovery of corticosteroids, MV was used therapeutically to treat autoimmune nephrotic syndrome (5). Furthermore, this suppression of immune function has long been appreciated as a major cause for the high mortality of currently over 1 million deaths per year and morbidity of currently over 40 million cases per year from MV infection (6, 7). These observations are firm, as is previous research documenting that MV infects cells of the immune system (8–16), interferes with cellular and humoral immune responses and lymphoid proliferation (for reviews see refs. 1 and 17–20) and causes cell cycle arrest in late G1 of infected T and B lymphocytes (21–23), but does not shut down protein synthesis of infected cells (23–26). However the mechanism(s) and molecules involved in the initiation and maintenance of this process have been poorly understood. The paper by Schlender et al. …