Unlike T and NK cells, B cells had the ability to increase surface expression of the early activation marker CD69 in response to ZIKV infection of total PBMC; however, this upregulation was significantly diminished after experimental depletion of pDCs, suggesting that functional connections between pDCs and B cells are necessary to effectively activate B cells following ZIKV exposure (Fig. 6d and Supplementary Fig. 5d). The gene discussed is CD69; the disease is Zika virus infectious disease.