Since we observed a significant time-dependent activation of NF-κB p65 subunit in hBMECs along with the infection (Figure 2B), which was exactly consistent with our previous data [21,22], we next investigated the effects of miR-19b-3p overexpression or inhibition on the phosphorylation of NF-κB p65 subunit, as well as on the generation of proinflammatory cytokines and chemokines in response to the infection. This evidence concerns the gene NFKB1 and infection.