Infected monocytes/macrophages and CD4+ lymphocytes could also facilitate productive viral replication in this region [56,58], providing a source of infection for brain microvascular endothelial cells, which in turn may exacerbate the BBB permeabilization via the degradation of inter-endothelial tight junctions and upregulation of CAM expression [32,46]. The gene discussed is CD4; the disease is infection.