Cell tropism for vaccine and wild-type MV strains is largely determined by virus entry (Tatsuo et al. 2000a ). Wild-type MV, which use predominantly SLAM/CD150 expressed on activated immune cells (Tatsuo et al. 2000b) , is known to mainly replicate in lymphoid organs and epithelial tissues such as the skin, respiratory tract, intestine and urinary bladder (Griffin 2007; Takeda 2008) . Recent studies suggest that after aerosol infection, wild-type MV initially targets macrophages and dendritic cells in alveolar tissues, which is followed by replication in regional lymph nodes and systemic spreading to lymphoid organs (Lemon et al. 2011) . How MV infects CD150-negative epithelial cells remains largely unclear, although putative epithelial receptors have recently been described (Watanabe et al. 2010) . As MV vaccine strains use the ubiquitous CD46 receptor in addition to the receptors used by wild-type MV (Dorig et al. 1993) , the vaccine strains were expected to exhibit a wider tropism than that documented previously for wild-type MV (Griffin 2007; Lemon et al. 2011; Takeda 2008) . However, in macaques infected intratracheally or by aerosol with wild-type or attenuated (Edmonston tag) recombinant MV, only the pathogenic MV caused significant viremia and widespread distribution. The attenuated MV had a restricted systemic spread and was rarely detected in lymphoid tissues (de Vries et al. 2010) , in contrast to observations in the current study. Our data seem to be more aligned with studies in mice immunized intraperitoneally or intravenously with an attenuated oncolytic (Edmonston) recombinant strain, in which infected cells were mainly detected in secondary lymphoid organs, liver and lungs (Myers et al. 2007; Peng et al. 2003) . These disparities between studies may be explained by differences in administration routes, MV strains or methods of MV detection.