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

doi:10.1038/ni818

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

Research output: Contribution to journal › Article › peer-review

148 Citations (Scopus)

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.

Original language	English
Pages (from-to)	733-740
Number of pages	8
Journal	Nature Immunology
Volume	3
Issue number	8
DOIs	https://doi.org/10.1038/ni818
Publication status	Published - 8 Jul 2002
Externally published	Yes

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title = "K3-mediated evasion of CD8+ T cells aids amplification of a latent γ-herpesvirus",

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.",

author = "Stevenson, {P. G.} and May, {J. S.} and Smith, {X. G.} and S. Marques and H. Adler and Koszinowski, {U. H.} and Simas, {J. P.} and S. Efstathiou",

note = "Funding Information: Acknowledgments We thank P. C. Doherty, S.Andreansky,A. C. Minson, B. Smillie and A. Hancock. Supported by the Wellcome Trust (grant 059601 to P. G. S. and S. E.), the MRC (grants G108/462 and G9901295 of G9800943 to P. G. S.), the FCT (grant Praxis/10265/98 to S. M. and J. P. S.) and the BMBF (grant FKZ 01K1960612) and DFG (grant sAd121/2-1 and SFB 455) (to H. A. and U. H. K.).",

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AU - Stevenson, P. G.

AU - May, J. S.

AU - Smith, X. G.

AU - Marques, S.

AU - Adler, H.

AU - Koszinowski, U. H.

AU - Simas, J. P.

AU - Efstathiou, S.

N1 - Funding Information: Acknowledgments We thank P. C. Doherty, S.Andreansky,A. C. Minson, B. Smillie and A. Hancock. Supported by the Wellcome Trust (grant 059601 to P. G. S. and S. E.), the MRC (grants G108/462 and G9901295 of G9800943 to P. G. S.), the FCT (grant Praxis/10265/98 to S. M. and J. P. S.) and the BMBF (grant FKZ 01K1960612) and DFG (grant sAd121/2-1 and SFB 455) (to H. A. and U. H. K.).

PY - 2002/7/8

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N2 - 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.

AB - 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.

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

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