During footpad infection with ectromelia virus, the administration of an anti-Bst2 antibody to deplete pDCs in Batf3-KO mice constitutively lacking cDC1s was sufficient to induce a dramatic increase in infection-induced death, whereas neither of these two deficiencies alone significantly increased mouse mortality, supporting redundancies between pDC and cDC1 functions to control this viral infection in vivo [107]. This evidence concerns the gene BST2 and infection.