Abstract
Although CNS complications occuring early and late after acute measles are a serious problem and often fatal, the transient immunosuppression lasting for several weeks after the rash is the major cause of measles-related morbidity and mortality worldwide. This review is focused on the interactions of measles virus (MV) with cellular receptors on neural and lymphoid cells which are important elements in viral pathogenesis. First, the cognate MV receptors, CD46 and CD150, are important components of viral tropism by mediating binding and entry. Second, however, additional unknown cellular surface molecules may (independently of viral uptake) after interaction with the MV glycoprotein complex act as signaling molecules and thereby modulate cellular survival, proliferation, and specific functions.