While secondary infection with dengue virus led to increases of CD4+ T cells and T cell subsets, which are involved in adaptive immunity, secondary infection with Zika virus induced the upregulation of several functional markers including IFNγ and macrophage inflammatory protein-1β (MIP-1β) in NK cells, DCs, and monocytes, indicating an intact innate immunity against Zika virus in the cases of possible concurrent dengue infection. This evidence concerns the gene CD4 and infection.