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Cytomegalovirus vectors violate CD8+ T cell epitope recognition paradigms.

Authors
  • Hansen, Scott G
  • Sacha, Jonah B
  • Hughes, Colette M
  • Ford, Julia C
  • Burwitz, Benjamin J
  • Scholz, Isabel
  • Gilbride, Roxanne M
  • Lewis, Matthew S
  • Gilliam, Awbrey N
  • Ventura, Abigail B
  • Malouli, Daniel
  • Xu, Guangwu
  • Richards, Rebecca
  • Whizin, Nathan
  • Reed, Jason S
  • Hammond, Katherine B
  • Fischer, Miranda
  • Turner, John M
  • Legasse, Alfred W
  • Axthelm, Michael K
  • And 5 more
Type
Published Article
Journal
Science
Publisher
American Association for the Advancement of Science (AAAS)
Publication Date
May 24, 2013
Volume
340
Issue
6135
Pages
1237874–1237874
Identifiers
DOI: 10.1126/science.1237874
PMID: 23704576
Source
Medline
License
Unknown

Abstract

CD8(+) T cell responses focus on a small fraction of pathogen- or vaccine-encoded peptides, and for some pathogens, these restricted recognition hierarchies limit the effectiveness of antipathogen immunity. We found that simian immunodeficiency virus (SIV) protein-expressing rhesus cytomegalovirus (RhCMV) vectors elicit SIV-specific CD8(+) T cells that recognize unusual, diverse, and highly promiscuous epitopes, including dominant responses to epitopes restricted by class II major histocompatibility complex (MHC) molecules. Induction of canonical SIV epitope-specific CD8(+) T cell responses is suppressed by the RhCMV-encoded Rh189 gene (corresponding to human CMV US11), and the promiscuous MHC class I- and class II-restricted CD8(+) T cell responses occur only in the absence of the Rh157.5, Rh157.4, and Rh157.6 (human CMV UL128, UL130, and UL131) genes. Thus, CMV vectors can be genetically programmed to achieve distinct patterns of CD8(+) T cell epitope recognition.

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