Immune evasion proteins gpUS2 and gpUS11 of human cytomegalovirus incompletely protect infected cells from CD8 T cell recognition

Abstract Human cytomegalovirus (HCMV) encodes four glycoproteins, termed gpUS2, gpUS3, gpUS6 and gpUS11 that interfere with MHC class I biosynthesis and antigen presentation. Despite gpUS2–11 expression, however, HCMV infection is efficiently controlled by cytolytic CD8 T lymphocytes (CTL). To addre...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2009-08, Vol.391 (1), p.5-19
Main Authors: Besold, K, Wills, M, Plachter, B
Format: Article
Language:English
Subjects:
Antigen Presentation - immunology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
CD8-Positive T-Lymphocytes - virology
Cells, Cultured
CTL
Cytomegalovirus
Cytomegalovirus - genetics
Cytomegalovirus - immunology
Cytomegalovirus - physiology
Cytomegalovirus Infections - immunology
Cytomegalovirus Infections - virology
HLA-A2 Antigen - immunology
HLA-B7 Antigen - immunology
Human cytomegalovirus
Humans
IE1
Immediate-Early Proteins - immunology
Immune evasion
Infectious Disease
Interferon-gamma - metabolism
MHC class I
Mutagenesis
Phosphoproteins - immunology
pp65
RNA-Binding Proteins - genetics
RNA-Binding Proteins - immunology
US11
US2
Viral Envelope Proteins - genetics
Viral Envelope Proteins - immunology
Viral Matrix Proteins - immunology
Viral Proteins - genetics
Viral Proteins - immunology
Virus Replication
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Summary:Abstract Human cytomegalovirus (HCMV) encodes four glycoproteins, termed gpUS2, gpUS3, gpUS6 and gpUS11 that interfere with MHC class I biosynthesis and antigen presentation. Despite gpUS2–11 expression, however, HCMV infection is efficiently controlled by cytolytic CD8 T lymphocytes (CTL). To address the role of gpUS2 and gpUS11 in antigen presentation during viral infection, HCMV mutants were generated that expressed either gpUS2 or gpUS11 alone without coexpression of the three other proteins. Fibroblasts infected with these viruses showed reduced HLA-A2 and HLA-B7 surface expression. Surprisingly, however, CTL directed against the tegument protein pp65 and the regulatory IE1 protein still recognized and lysed mutant virus infected fibroblasts. Yet, suppression of IE1 derived peptide presentation by gpUS2 or gpUS11 was far more pronounced. The results show that gpUS2 and gpUS11 alone only incompletely protect HCMV infected fibroblasts from CTL recognition and underline the importance of studying infected cells to elucidate HCMV immune evasion.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2009.06.004