Abstract
Replication of mouse hepatitis virus strain JHM (JHMV) in the central nervous system (CNS) is controlled by CD8+ T cells. However, persistent infection and subsequent chronic demyelination are established. Understanding effector mechanisms during acute infection may help understand viral persistence. CD8+ T cells respond to viral infections via two different cellular mechanisms, lysis of infected cells and secretion of anti-viral cytokines (Kaki et al 1995, Ruby et al 1991, Young et al 1995). JHMV replication in astrocytes and microglia is controlled by perforin-dependent cytolysis (Lin et al 1997) whereas replication in oligodendrocytes is controlled via IFN-γ (Parra et al 1999). The contributions of IFN-γ and perforin-dependent CD8+ T cell function in viral clearance were examined in SCID mice following adoptive transfer of CD8+ T cells deficient in IFN-γ secretion.
Chapter PDF
Similar content being viewed by others
Keywords
- SCID Mouse
- Viral Clearance
- Central Nervous System Cell
- Central Nervous System Cell Type
- Infected SCID Mouse
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
References
Kagi, D., Seiler, P., Pavlovic, P., Ledermann, B., Burki, K., Zinkernagel, R. M., and Hengatner, H., 1995, The roles of perform and fas-dependent cytotoxicity in protection against cytopathic and non cytophatic viruses. Eur. J. Immunol. 25:3256–3262.
Ruby, J., and Ramshaw, I., 1991, The antiviral activity of immune CD8+ T cells is dependent on interferon-y. Lymphokine Cytokine Res. 10:353–358.
Young, H. A., and Hardy, K. J., 1995, Role of interferon-y in immune cell regulation. J. Leukoc.Biol. 58:373–381.
Lin, M. T., Stohlman, S. A., and Hinton, D. R., 1997, Mouse hepatitis virus is cleared from the central nervous systems of mice lacking perforin-mediated cytolysis. J. Virol. 71:383–391.
Parra, B., Hinton, D. R., Marten, N. W., Bergmann, C. C., Lin, M. T., Yang, C. S., and Stohlman, S. A., 1999, IFN-γ is required for viral clearance from central nervous system Oligodendroglia. J. Immunol. 162:1641–1647.
Fleming, J. O., Trousdale, M. D., el-Zaatari, F. A., Stohlman, S. A., and Weiner, L. P., 1986 Pathogenicity of antigenic variants of murine Coronavirus JHM selected with monoclonal antibodies. J. Virol. 58:869–875.
Bergmann, C. C., Airman, J. D., Hinton, D., and Stohlman, S. A., 1999, Inverted Immunodominance and Impaired Cytolytic Function of CD8+ T Cells During Viral Persistence in the Central Nervous System. J. Immunol. 163:3379–3387.
Stohlman, S. A., Bergmann, C. C., van der Veen, R., and Hinton, D. R., 1995 Mouse hepatitis virus-specific cytotoxic T lymphocytes protect from lethal infection without eliminating virus from Oligodendroglia. J. Virol. 69:684–694.
Graham, M. B., Dalton, D. K., Giltinan, D., Braciale, V. L., Stewart, T. A., and Braciale, T. J., 1993, Response to influenza infection in mice with a targeted disruption in the interferon γ gene. J. Exp. Med. 178:1725–1732.
Nansen, A., Christensen, J. P., Ropke, C., Marker, O., Scheynius, A., and Thomsen, A. R., 1998, Role of interferon-γ in the pathogenesis of LCMV-induced meningitis: unimpaired leukocyte recruitment, but deficient macrophage activation in interferon-γ knock-out mice. J. Neuroimmunol. 86:202–212.
Njenja, M. K., Pease, L. R., Wettstein, P., Mark, T., and Rodriguez, M., 1997, Interferon γ mediates early-virus induced expression of H2d and H2k in the central nervous system. Lab. Invest. 77:71–84.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2001 Springer Science+Business Media New York
About this chapter
Cite this chapter
Parra, B., Bergmann, C.C., Hinton, D.R., Atkinson, R., Stohlman, S.A. (2001). IFN-γ Secreted by Virus-Specific CD8+ T Cells Contribute to CNS Viral Clearance. In: Lavi, E., Weiss, S.R., Hingley, S.T. (eds) The Nidoviruses. Advances in Experimental Medicine and Biology, vol 494. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1325-4_50
Download citation
DOI: https://doi.org/10.1007/978-1-4615-1325-4_50
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5498-7
Online ISBN: 978-1-4615-1325-4
eBook Packages: Springer Book Archive