*4.3. Pathogenesis*

Pathogenesis starts with MeV infection of myeloid cells in the respiratory tract. As mentioned in Section 2, the two known entry receptors forMeV wild-type strains are SLAM/CD150 and nectin-4 [18,19]. Wild-type (wt) viruses generally target lung resident macrophages and/or dendritic cells, expressing SLAM [62–64]. These antigen presenting cells (APCs) migrate to the lymph nodes and transmit the viral infection to SLAM expressing lymphocytes with subsequent spread of the virus in the lymphatic and vascular systems (viremia). During the late stages of the infection, circulating infected immune cells that reach the respiratory tract and the skin can transmit the infection in cis to epithelial cells expressing nectin-4 on their basolateral side [20,65–67]. Then, the virions produced at the apical membrane can be shed into the respiratory mucus or aerosolized in the respiratory tract through coughing [68].
