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Hantaviral mechanisms driving HLA class I antigen presentation require both RIG-I and TRIF.

Authors
  • 1
  • 1 Institute of Medical Virology, Charité-Universitätsmedizin Berlin, Berlin, Germany. , (Germany)
Type
Published Article
Journal
European Journal of Immunology
1521-4141
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
43
Issue
10
Pages
2566–2576
Identifiers
DOI: 10.1002/eji.201243066
PMID: 23824566
Source
Medline
Keywords
License
Unknown

Abstract

Hantaviruses are emerging human pathogens. They induce an unusually strong antiviral response of human HLA class I (HLA-I) restricted CD8⁺ T cells that may contribute to tissue damage and hantavirus-associated disease. In this study, we analyzed possible hantaviral mechanisms that enhance the HLA-I antigen presentation machinery. Upon hantavirus infection of various human and primate cell lines, we observed transactivation of promoters controlling classical HLA molecules. Hantavirus-induced HLA-I upregulation required proteasomal activity and was associated with increased TAP expression. Intriguingly, human DCs acquired the capacity to cross-present antigen upon hantavirus infection. Furthermore, knockdown of TIR domain containing adaptor inducing IFN-β or retinoic acid inducible gene I abolished hantavirus-driven HLA-I induction. In contrast, MyD88-dependent viral sensors were not involved in HLA-I induction. Our results show that hantaviruses strongly boost the HLA-I antigen presentation machinery by mechanisms that are dependent on both retinoic acid inducible gene I and TIR domain containing adaptor inducing IFN-β.

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