Receptor interactions, tropism, and mechanisms involved in morbillivirus-induced immunomodulation.

Induction of immunomodulation and -suppression is a common feature of morbilliviruses such as measles virus (MV), rinderpest virus (RPV), and canine distemper virus (CDV) in their respective hosts. As major uptake receptor, signaling lymphocytic activation molecule (SLAM, CD150) essentially determines their tropism for immune cells, which is of considerable importance with regard to immunosuppression and the systemic spread to organs including secondary lymphoid organs, the skin, the respiratory tract, and the brain. Independent of their ability to enhance virus uptake in specialized host cells, other cell surface receptors such as the substance P receptor, DC-SIGN, Toll-like receptors (TLR), Fc-gamma receptor II (FcgammaRII), CD46, and additional uncharacterized receptors exert a variety of immunomodulatory effects as reflected by activation of or interference with viability, differentiation, trafficking, or acquisition of effector functions of specialized immune cells. In this review, we discuss receptor interactions, tropism, and mechanisms involved in the severe, transient immunosuppression induced by MV and other morbilliviruses.