K3-mediated evasion of CD8(+) T cells aids amplification of a latent gamma-herpesvirus - PubMed (original) (raw)
doi: 10.1038/ni818. Epub 2002 Jul 8.
Affiliations
- PMID: 12101398
- DOI: 10.1038/ni818
K3-mediated evasion of CD8(+) T cells aids amplification of a latent gamma-herpesvirus
P G Stevenson et al. Nat Immunol. 2002 Aug.
Abstract
The murine gamma-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.
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