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Characterization of Human T Cell Clones Specific for Coronavirus 229E

  • J. S. Spencer
  • G. F. Cabirac
  • C. Best
  • L. McLaughlin
  • R. S. Murray
Chapter
  • 210 Downloads
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 380)

Abstract

Coronaviruses (CV) are pleomorphic enveloped RNA viruses that are ubiquitous in nature, causing a variety of diseases in both man and domestic animals. In man, CV are generally associated with upper respiratory tract infections. The two prototype strains that are the best studied human CV isolates and which are thought to be responsible for most of the respiratory infections caused by CV are called 229E and OC43. Humoral responses consisting of neutralizing antibodies to CV are present in most individuals by six years of age. Although the cellular immune response to CV in man has not been characterized at all, it is known that the spike (S) and nucleocapsid (N) proteins elicit the major cell mediated immune responses in the mouse.

This report describes the production and characterization of eleven independently isolated T cell clones that are specific for the human CV(HCV) 229E. The T cell clones are CD4+ and presumably recognize a processed viral peptide presented by class II molecules on the surface of antigen presenting cells. Of six 229E-specific T cell clones tested against purified viral proteins, three recognize the 180 kD spike glycoprotein while the other three recognize the 55 kD nucleocapsid phosphoprotein. Analysis of the human T cell mediated response to HCV will provide information regarding which viral proteins elicit the immunodominant response, what the fine specificity of these T cell clones are (immuno-dominant peptides), and what the T cell receptor (TCR) and cytokine usage is of these virus specific clones.

Keywords

Epstein Barr Virus Multiple Sclerosis Patient Cell Clone Lyme Disease Cell Mediate Response 
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

  1. 1.
    Zamvil, S.S., and L. Steinman. The T lymphocyte in experimental allergic encephalomyelitis. Annu. Rev. Immunol. 1990; 8:579.PubMedCrossRefGoogle Scholar
  2. 2.
    Acha-Orbea, H., D.J. Mitchell, L. Timmermann, D.C. Wraith, and G.S. Tausch. Limited heterogeneity of T cell receptors from lyphocytes mediating autoimmune encephalomyelitis allows specific immune intervention. Cell. 1988; 54:263.PubMedCrossRefGoogle Scholar
  3. 3.
    Ben-Nun, A., H. Wekerle, and I.R. Cohen. Vaccination against autoimmune encephalomyelitis with T-lymphocyte line cells reactive against myelin basic protein. Nature. 1981; 293:60.CrossRefGoogle Scholar
  4. 4.
    Martin, R., H.F. McFarland, and D.E. McFarlin. Immunologic aspects of demyelinating diseases. Annu. Rev. Immunol. 1992; 10:153.PubMedCrossRefGoogle Scholar
  5. 5.
    Booss, J., and J.H. Kim. Evidence for a viral etiology of multiple sclerosis. In: “Handbook of Multiple Sclerosis”, S.D. Cook, ed. Marcel,Dekker, Inc., New York. 1990; pp 41–61.Google Scholar
  6. 6.
    Mcintosh, K. Coronaviruses. In: “Virology”, B.N. Fields, et al., eds. Raven Press, New York. 1985; pp 1323–1330.Google Scholar
  7. 7.
    Hamre, D., and M. Beem. Virologic studies of acute respiratory disease in young adults. V. Coronavirus 229E infections during six years of surveillance. Am. J. Epidemiol. 1972; 96:94.PubMedGoogle Scholar
  8. 8.
    Resta, S., J.P. Luby, C.R. Rosenfeld, and J.D. Siegel. Isolation and propagation of a human enteric coronavirus. Science. 1985; 229:978.PubMedCrossRefGoogle Scholar
  9. 9.
    Battaglia, M., N. Passarini, A. DiMatteo, and G. Gerna. Human enteric coronaviruses: further charac-terization and immunoblotting of viral proteins. J. Inf. Dis. 1987; 155:140.CrossRefGoogle Scholar
  10. 10.
    Malkova, D., J. Holubova, J.M. Kolman, F. Lobkovic, L. Pohlreichova, and L. Zikmundova. Isolation of Tettnang coronavirus from man? Acta Virol. (Prague)(Eng. Ed.) 1980; 24:363.Google Scholar
  11. 11.
    Tanaka, R., Y. Iwasaki, and H.J. Koprowski. Ultrastructural studies of perivascular cuffing cells in multiple sclerosis brain. J. Neurol. Sci. 1976; 28:121.PubMedCrossRefGoogle Scholar
  12. 12.
    Burks, J.S., B.L. Devald, L.D. Jankovsky, and J.D. Gerdes. Two coronaviruses isolated from central nervous system tissue of two muliple sclerosis patients. Science. 1980; 209:933.PubMedCrossRefGoogle Scholar
  13. 13.
    Gerdes, J.C., I. Klein, B.L. DeVald, and J.S. Burks. Coronavirus isolates SK and SD from multiple sclerosis patients are serologically related to murine coronaviruses A59 and JHM and human coronavirus OC43, but not to human coronavirus 229E. J. Virol. 1981; 38:231.PubMedGoogle Scholar
  14. 14.
    Murray, R.S., B. Brown, D.A. Brian, and G.R Cabirac. Detection of coronavirus RNA and antigen in multiple sclerosis brain. Ann. Neurol. 1992; 31:525.PubMedCrossRefGoogle Scholar
  15. 15.
    Stewart, J.N., S. Mounir, and P.J. Talbot. Human coronavirus gene expression in the brains of multiple sclerosis patients. Virology. 1992; 191:502.PubMedCrossRefGoogle Scholar
  16. 16.
    Talbot, P.J., S. Ekande, N.R. Cashman, S. Mounir, and J.N. Stewart. Neurotropism of human coronavirus 229E. In: Adv. in Exp. Med. and Biol., H. Laude and J-F. Vautherot, eds. Plenum Press, New York. 1993; 342:339.Google Scholar
  17. 17.
    Murray, R.S., G-Y. Cai, K. Hoel, J-Y. Zhang, K.F. Soike, and G.F. Cabirac. Coronavirus infects and causes demyelination in primate central nervous system. Virology. 1992; 188:274.PubMedCrossRefGoogle Scholar
  18. 18.
    Fleming, J.O., M.D. Trowsdale, J. Bradbury, S.A. Stohlman, and L.P. Weiner. Experimental demyelination induced by coronavirus JHM (MHV-4). Molecular identification of a viral paralytic disease. Microb. Path. 1987; 3:9.CrossRefGoogle Scholar
  19. 19.
    Wege, H., S.G. Siddell, and V Ter Meulen. The biology and pathogenesis of coronaviruses. Curr. Top. Microbiol. Immunol. 1982; 99:165.PubMedCrossRefGoogle Scholar
  20. 20.
    Nagashima, K., H. Wege, R. Meyermann, and V. Ter Meulen. Demyelinating encephalomyelitis induced by a long term coronavirus infection in rats. Acta Neuropath. 1979; 45:205.PubMedCrossRefGoogle Scholar
  21. 21.
    Kyuwa, S., and S.A. Stohlman. Pathogenesis of a neurotropic murine coronavirus, strain JHM, in the central nervous system of mice. Semin. Vir. 1990; 1:273.Google Scholar
  22. 22.
    Williamson, J.S.P., and S.A. Stohlman. Effective clearance of mouse hepatitis virus from the central nervous system requires both CD4+ and CD8+ T cells. J. Virol. 1990; 64:4589.PubMedGoogle Scholar
  23. 23.
    Korner, H., A. Schiephake, J. Winter, F. Zimprich, H. Lassmann, J. Sedgwick, S. Siddell, and H. Wege. Nucleocapsid or spike protein specific CD4+ T lymphocytes protect against coronavirus-induced encephalomyelitis in the absence of CD8+ T cells. J. Immunol. 1991; 147:2317.PubMedGoogle Scholar
  24. 24.
    Stohlman, S.A., and L.P. Weiner. Chronic nervous system demyelination in mice after JHM virus infection. Neurology. 1981; 31:38.PubMedCrossRefGoogle Scholar
  25. 25.
    Hirano, N., K. Fugiwara, S. Hino, and M. Matumoto. Replication and plaque formation of mouse hepatitis virus (MHV-2) in mouse cell line DBT culture. Arch. Gesamte Virusforsch. 1974; 44:298.PubMedCrossRefGoogle Scholar
  26. 26.
    Weiss, S. Coronavirus SD and SK share extensive nucleotide homology with murine coronavirus MHV-A59 more than that shared between human and murine coronaviruses. Virology. 1983; 126:669.PubMedCrossRefGoogle Scholar
  27. 27.
    Bergmann, C., M. McMillan, and S. Stohlman. Characterization of the Ld-restricted cytotoxic T-lymphocyte epitope in the mouse hepatitis virus nucleocapsid protein. J. Virol. 1993; 67:7041.PubMedGoogle Scholar
  28. 28.
    Oksenberg, J.R., M.A. Panzara, A.B. Begovich, D. Mitchell, H.A. Erlich, R.S. Murray, R. Shimonkevitz, M. Sherritt, J. Rothbard, C.C.A. Bernard, and L. Steinman. Selection for T-cell receptor Vβ-Dβ-Jβ gene rearrangements with specificity for a myelin basic protein peptide in brain lesions of multiple sclerosis. Nature. 1993; 362:68.PubMedCrossRefGoogle Scholar
  29. 29.
    Wucherpfennig, K.W., K. Ota, N. Endo, J.G. Seidman, A. Rosenzweig, H.L. Weiner, and D.A. Hafler. Shared human T cell receptor usage to immunodominant regions of myelin basic protein. Science. 1990; 248:1016.PubMedCrossRefGoogle Scholar
  30. 30.
    Lahesmaa, R., M-C. Shanafelt, A. Allsup, C. Soderberg, J. Anzola, V Freitas, C. Turck, L. Steinman, and G. Peltz. Preferential usage of T cell antigen receptor V region gene segment Vp5.1 by Borrelia burgdorferi antigen-reactive T cell clones isolated from a patient with Lyme disease. J. Immunol. 1993; 150:4125. PubMedGoogle Scholar
  31. 31.
    Paliard, X., S.G. West, J.A. Lafferty, J.R. Clements, J.W. Kappler, P. Marrack, and B.L. Kotzin. Evidence for the effects of a superantigen in rheumatoid arthritis. Science. 1991; 253:325.PubMedCrossRefGoogle Scholar
  32. 32.
    Conrad, B., E. Weidmann, G. Trucco, W.A. Rudert, R. Behboo, C. Ricordi, H. Rodriquez-Rilo, D. Finegold, and M. Trucco. Evidence for superantigen involvement in insulin-dependent diabetes mellitus aetiology. Nature. 1994; 371:351.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • J. S. Spencer
    • 1
    • 3
  • G. F. Cabirac
    • 1
    • 2
    • 4
  • C. Best
    • 1
  • L. McLaughlin
    • 1
  • R. S. Murray
    • 2
    • 5
  1. 1.Rocky Mountain Multiple Sclerosis CenterUSA
  2. 2.Colorado Neurological InstituteEnglewoodUSA
  3. 3.Department of ImmunologyUSA
  4. 4.Department of Biochemistry, Biophysics and GeneticsUniversity of Colorado Health Sciences CenterDenverUSA
  5. 5.National Jewish Center for Immunology and Respiratory MedicineDenverUSA

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