Two mechanisms of MV entry were proposed based on these findings: infection of CD150+ cells in the alveolar spaces or binding to dendrites of DC-SIGN+ submucosal DCs in the lumen of the respiratory tract, followed by migration to tertiary lymphoid tissues, such as the bronchus-associated lymphoid tissue [24], and draining lymph nodes [8,25,26], where the infection is subsequently amplified by massive replication in abundantly present CD150+ B- and T-cells [8,27]. Here, SLAMF1 is linked to infection.