TY - JOUR
T1 - Herpesviruses and immunity
T2 - The art of evasion
AU - Griffin, Bryan D.
AU - Verweij, Marieke C.
AU - Wiertz, Emmanuel J.H.J.
N1 - Funding Information:
We thank the Dutch Cancer Society (grant UL 2005-3259) and the Macropa Foundation, Leiden, for financial support.
PY - 2010/6
Y1 - 2010/6
N2 - Herpesviruses have evolved several effective strategies to counter the host immune response. Chief among these is inhibition of the host MHC class I antigen processing and presentation pathway, thereby reducing the presentation of virus-derived epitopes on the surface of the infected cell. This review summarizes the mechanisms used by herpesviruses to achieve this goal, including shut-down of MHC class I molecule synthesis, blockage of proteasome-mediated peptide generation and prevention of TAP-mediated peptide transport. Furthermore, herpesvirus proteins can retain MHC class I molecules in the endoplasmic reticulum, or direct their retrograde translocation from the endoplasmic reticulum or endocytosis from the plasma membrane, with subsequent degradation. The resulting down-regulation of cell surface MHC class I peptide complexes thwarts the ability of cytotoxic T lymphocytes to recognize and eliminate virus-infected cells. The subversion of the natural killer cell response by herpesvirus proteins and microRNAs is also discussed.
AB - Herpesviruses have evolved several effective strategies to counter the host immune response. Chief among these is inhibition of the host MHC class I antigen processing and presentation pathway, thereby reducing the presentation of virus-derived epitopes on the surface of the infected cell. This review summarizes the mechanisms used by herpesviruses to achieve this goal, including shut-down of MHC class I molecule synthesis, blockage of proteasome-mediated peptide generation and prevention of TAP-mediated peptide transport. Furthermore, herpesvirus proteins can retain MHC class I molecules in the endoplasmic reticulum, or direct their retrograde translocation from the endoplasmic reticulum or endocytosis from the plasma membrane, with subsequent degradation. The resulting down-regulation of cell surface MHC class I peptide complexes thwarts the ability of cytotoxic T lymphocytes to recognize and eliminate virus-infected cells. The subversion of the natural killer cell response by herpesvirus proteins and microRNAs is also discussed.
KW - Antigen presentation
KW - Herpesvirus
KW - Immune evasion
KW - MHC class I molecule
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U2 - 10.1016/j.vetmic.2010.02.017
DO - 10.1016/j.vetmic.2010.02.017
M3 - Review article
C2 - 20303681
AN - SCOPUS:77952857516
SN - 0378-1135
VL - 143
SP - 89
EP - 100
JO - Veterinary Microbiology
JF - Veterinary Microbiology
IS - 1
ER -