While low-dose HSV-1 infection in human myeloid dendritic cells (DC) increases surface CD1d expression (51, 57), infection with high-viral titers triggers the rapid re-distribution of surface CD1d molecules to the limiting membrane of lysosomes and the trans-Golgi network (Figure 1), an action mediated by HSV-1 glycoprotein B (gB) and the viral serine–threonine kinase, US3, which inhibits the activation of iNKT cells (26, 58). This evidence concerns the gene CD1D and infection.