The pathogenesis of measles revisited

Abstract

Measles continues to be an important cause of childhood mortality in developing countries. The causative agent, measles virus (MV), is a member of the family Paramyxoviridae, genus Morbillivirus, and is spread via the respiratory route. MV was originally thought to enter the host by infecting epithelial cells of the respiratory tract, followed by viremia mediated by infected monocytes. However, neither of these cell types express signaling lymphocyte activation molecule (SLAM, CD150), which has been identified as the main receptor for wild-type MV. Measles has a relatively long incubation time, which makes it difficult to study the early stages of MV infection in humans. The animal models that best reflect the pathogenesis of measles are based on nonhuman primates. The use of recombinant MV strains expressing fluorescent proteins has greatly facilitated studies on viral tropism in macaques. These studies indicate that dendritic cells and lymphocytes expressing CD150 are the primary target cells for MV infection. At late stages of the infection MV also infects epithelial cells, despite the fact that these do not express CD150. Whether these cells express an as yet unidentified additional MV receptor remains unclear. On basis of these data it could be envisaged that dendritic cells are the first target cells for MV infection. These antigen-presenting cells may traffic the virus to the regional lymph nodes where they can transmit the virus to lymphocytes, which during viremia disseminate the virus throughout the body.