The infection, which passed through BMEC, gave significant cytopathic effects and an acute lytic infection together with BMEC cell apoptosis and a reduction of brain–barrier activity after the end of the infectious time, that could also occur in vivo [126].Moreover, a recent study has shown the presence of HCV receptors (including CD68, CD81, claudin-1, LDLR, and scavenger receptor-B1) on the brain microvasculature, representing a gate through which the virus can infect brain cells [126]. The gene discussed is CLDN1; the disease is infection.