Our results support the following conclusions: (1) EV71 prefers to proliferate in the CD141+ and CD11b+ subsets of the pre-cDC population and to use these cells for its transmission during the early stages of infection in rhesus macaques and, (2) the proliferation and transmission of EV71 in these specific DC subsets during the infective process is not involved in the pathogenesis of the viral infection, nor does it interfere with the development of an independent immune response against EV71. This evidence concerns the gene ITGAM and infection.