Human cytomegalovirus (HCMV), a prototypical beta-herpes virus, is a major cause of morbidity and mortality in immunocompromised transplant recipients and congenitally infected fetuses.Different HCMV glycoprotein complexes are capable of meditating entry through interaction with cell-specific receptors on a panel of host cells. The pentamer (gH/gL/UL128/UL130/UL131A) mediates HCMV entry into epithelial, endothelial, and myeloid cells by its binding to neuropilin 2 (Nrp2). The trimer (gH/gL/gO) can mediate infection of all cell types by binding to platelet-derived growth factor-alpha (PDGFRα). Both pentamer and trimer need to interact with the glycoprotein B (gB), the fusogenic protein, to trigger the virus and host cell membrane fusion.