Human cytomegalovirus (HCMV) infects most individuals in the world, usually without producing overt symptoms. The broad cellular tropism of HCMV likely contributes to the diverse number of pathologies associated with infection.The deletion of glycoprotein B (gB) renders HCMV incapable of entering cells unless a chemical fusogen (ie polyethylene glycol) is added. HCMV gB has been shown to engage with a number of cellular receptors, including EGF-R, PDGF-Rα, tetherin and integrins (α2β1, α6β1 and αvβ3).  Synthesis of a protein on a ribosome (RIB) is digested  in the proteasome (PRO), transport of peptides into the endoplasmic reticulum (ER) by the transporter associated with antigenic peptides (TAP) and display, together with class I HLA molecules, at the plasma membrane. HCMV proteins pp65, UL97, US3, US6, US2 and US11 reduce display of mature class I complexes. HCMV proteins UL18 and UL40 present decoy signals to prevent immune attack. HCMV proteins UL16, UL141, UL142 plus micro-RNA UL112-1 block the display of stress ligands, which would otherwise precipitate immune attack.


1.Griffiths P,et al. J Pathol. 2015 Jan;235(2):288-97.