There is a paucity of information on dendritic cell (DC) responses to vaccinia virus (VACV), including the traffic of DCs to draining lymph node (dLN). Herein we studied skin DC migration in response to VACV and compared it to the tuberculosis vaccine Mycobacterium bovis Bacille Calmette-Guérin (BCG), another live-attenuated vaccine administered via the skin. In stark contrast to BCG, skin DCs did not relocate to dLN in response to VACV. Infection with UV-inactivated VACV or modified VACV Ankara (MVA) promoted DC movement to dLN, indicating that interference with skin DC migration requires replication-competent VACV. This suppressive effect of VACV was capable of mitigating responses to a secondary challenge with BCG in the skin, ablating DC migration, reducing BCG transport and delaying CD4+ T-cell priming in the dLN. Expression of inflammatory mediators associated with BCG-triggered DC migration were absent from virus-injected skin, suggesting that other pathways invoke DC movement in response to replication-deficient VACV. Despite adamant suppression of DC migration, VACV was still detected early in the dLN and primed Ag-specific CD4+ T cells. In summary, VACV blocks skin DC mobilization from the site of infection while retaining the ability to access the dLN to prime CD4+ T cells.