[1][2] Some viral immunoevasins block peptide entry into the endoplasmic reticulum (ER) by targeting the TAP transporters.
[4][5] Conversely to the HSV-1, the ATP-binding of TAP is inhibited by HCMV US6 protein, indirectly resulting in decreased peptide transport to ER.
[1][5][7] Nef protein is capable of directly binding to cytosolic regions of MHC I and targeting them for degradation in lysosomes from trans-Golgi.
[1] MHC II molecule (HLA-DR) acts as a co-receptor for the EBV entry into the cell upon binding the gp42 viral protein.
[1] BNLF2a protein, which is present only in the replicative phase of the viral life cycle, functions as an inhibitor of TAP, blocking both peptide and ATP binding.
[5] In the future, the use or knockouts of immunoevasins (where mutated or deleted immunoevasin genes would not interfere with antigen presentation on MHC I complexes upon viral infection, resulting in recognition and targeting of infected cells by T cells) may be used for vaccine development for HCMV, gene therapy, transplantation and tumor-specific immunotherapy.