K3-mediated evasion of CD8+ T cells aids amplification of a latent γ-herpesvirus

Stevenson, P. G., May, J. S., Smith, X. G., Marques, S., Adler, H., Koszinowski, U. H., Simas, J. P. and Efstathiou, S. (2002) K3-mediated evasion of CD8+ T cells aids amplification of a latent γ-herpesvirus. Nature Immunology, 3 8: 733-740. doi:10.1038/ni818


Author Stevenson, P. G.
May, J. S.
Smith, X. G.
Marques, S.
Adler, H.
Koszinowski, U. H.
Simas, J. P.
Efstathiou, S.
Title K3-mediated evasion of CD8+ T cells aids amplification of a latent γ-herpesvirus
Formatted title
K3-mediated evasion of CD8+ T cells aids amplification of a latent γ-herpesvirus
Journal name Nature Immunology   Check publisher's open access policy
ISSN 1529-2908
1529-2916
Publication date 2002-08-01
Year available 2002
Sub-type Article (original research)
DOI 10.1038/ni818
Open Access Status Not yet assessed
Volume 3
Issue 8
Start page 733
End page 740
Total pages 8
Place of publication New York, NY, United States
Publisher Nature Publishing Group
Language eng
Formatted abstract
The murine γ-herpesvirus-68 (MHV-68) K3 protein, like that of the Kaposi's sarcoma-associated herpesvirus, down-regulates major histocompatibility complex (MHC) class I expression. However, how this contributes to viral replication in vivo is unclear. After intranasal MHV-68 infection, K3 was transcribed both during acute lytic infection in the lung and during latency establishment in lymphoid tissue. K3-deficient viruses were not cleared more rapidly from the lung, but the number of latently infected spleen cells was reduced and the frequency of virus-specific CD8+ cytotoxic T lymphocytes (CTLs) was increased. CTL depletion reversed the viral latency deficit. Thus, a major function of K3 appears to be CTL evasion during viral latency expansion.
Keyword Immunology
Immunology
IMMUNOLOGY
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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