Indari O, et al. - In malaria-endemic countries, it is well established that Plasmodium (P.) falciparum infection mediates Epstein-Barr virus (EBV) reactivation. Researchers here examined if during malaria onset, the reactivated EBV can infect human brain microvascular endothelial cells (HBECs), which may cause severe cerebral manifestations. HBECs were infected with EBV in vitro. Using qRT-PCR, they identified that EBV infection of HBECs resulted in a significant elevation of several inflammatory (TNFα, CCL-2) and endothelial markers (Integrin β3, PECAM, VEGF-A, VWF, Claudin-5, Cx37). Significant reduction in the migration of HBECs, glial and neuronal cells was observed in correlation with secretion of EBV infected HBECs. From these findings, it can be concluded that the EBV infection of HBECs resulted in endothelial activation and modulated the BBB microenvironment. In addition, significantly increased RBC adhesion to HBECs was evident in correlation with EBV-P. falciparum co-infection which is a hallmark of cerebral malaria. In combination with malaria, the EBV infection can facilitate exacerbation of cerebral malaria pathology.