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

P. G. Stevenson, J. S. May, X. G. Smith, S. Marques, H. Adler, U. H. Koszinowski, J. P. Simas, S. Efstathiou

Resultado de pesquisarevisão de pares

147 Citações (Scopus)


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.
Idioma originalEnglish
Páginas (de-até)733-740
Número de páginas8
RevistaNature Immunology
Número de emissão8
Estado da publicaçãoPublished - 8 jul 2002
Publicado externamenteSim

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