Specifically, it has been shown that EBV infects human brain microvascular ECs (HBMECs) leading to EC activation and increased production of CCL-5 (RANTES) and the adhesion molecule, ICAM-1 in infected cells, suggesting that infected microvascular cells release inflammatory cytokines upon EBV infection (84). This evidence concerns the gene CCL5 and Epstein-Barr virus infection.