Our findings that THY-1 facilitates an early step of HCMV infection, and that down-regulation of THY-1 by siRNA or blocking THY-1 with antibody inhibits HCMV- induced PI3K-Akt activation within the initial 15–45 min of infection, suggests a pivotal role for THY-1 in the coupling of HCMV entry with host signaling, and supports observations that growth factor receptors (PDGFR- α and EGFR) engage integrin/paxilin pathways during HCMV infection [14,16,22,67]. This evidence concerns the gene AKT1 and cytomegalovirus infection.