1887

Abstract

Summary

BHK-21 cells readily produce tumours in athymic nude mice, but BHK-21 cells persistently infected with wild-type vesicular stomatitis virus (VSV) do not. However, rare persistently infected virus-shedding tumours (VSV-P tumour cells) were independently derived by selection on three different occasions. Cloned viruses isolated from each of these (VSV-P virus mutants) carried mutations determining the VSV-P phenotype because they all allowed growth of virus-shedding tumours in nude mice when they were used to persistently infect normal (unselected) BHK-21 cells. Treatment of nude mice with anti-asialo-GM1 allowed BHK cells persistently infected with wild-type VSV to form tumours, and BHK cells persistently infected with VSV-P were resistant to natural killer (NK) cells ; this implicates NK cells in the rejection of persistently infected tumours and in the selection of the VSV-P variant. In this paper, we have sequenced the glycoprotein (G protein), matrix (M) and non-structural (NS) proteins of three independently derived VSV-P type mutants to find mutations associated with passage of persistently infected nude mouse tumours and with resistance to NK cells. We found extensive mutation in the G protein of VSV-P but relatively few mutations in the M and NS proteins. This suggests but does not prove a role for the G protein in NK cell killing of infected cells.

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1986-03-01
2024-03-29
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References

  1. Bukowski J. F., Woda B. A., Haba S., Okumura K., Welsh R. M. 1983; Natural killer cell depletion enhances virus synthesis and virus induced hepatitis in vivo. Journal of Immunology 131:1531–1538
    [Google Scholar]
  2. Bukowski J. F., Warner J. F., Dennert G., Welsh R. 1985; Adoptive transfer studies demonstrating the antiviral effect of natural killer cells in vivo. Journal of Experimental Medicine 161:40–52
    [Google Scholar]
  3. Dietzschold B., Wunner W. H., Wiktor T. J., Lopes T. J., Lafon M., Smith C. L., Koprowski H. 1983; Characterization of an antigenic determinant of the glycoprotein that correlates with pathogenicity of rabies virus. Proceedings of the National Academy of Sciences, U.S.A 80:70–74
    [Google Scholar]
  4. Gallione C. J., Greene J. R., Iverson L. E., Rose J. K. 1981; Nucleotide sequence of the mRNA’s encoding the vesicular stomatitis virus N and NS proteins. Journal of Virology 39:529–535
    [Google Scholar]
  5. Gill D. S., Banerjee A. K. 1985; Vesicular stomatitis virus NS proteins: structural similarity without extensive sequence homology. Journal of Virology 55:60–66
    [Google Scholar]
  6. Habu S., Fukui H., Shimamura K., Kasai M., Nagai Y., Okumura K., Tamaoki N. 1981; In vivo effects of antiasialo GM1. I. Reduction of NK activity and enhancement of transplanted tumor growth in nude mice. Journal of Immunology 127:34–38
    [Google Scholar]
  7. Habu S., Shimamura K., Akamatsu K., Okumura K., Tamaoki N. 1984; Protective role of natural killer cells in tumour growth and viral infection in mice. Experimental Cell Research 52:40–43
    [Google Scholar]
  8. Holland J. J., Villarreal L. P. 1974; Persistent noncytocidal vesicular stomatitis virus infections mediated by defective T particles that suppress virion transcriptase. Proceedings of the National Academy of Sciences, U.S.A 71:2956–2960
    [Google Scholar]
  9. Holland J., Grabau E. A., Jones C. L., Semler B. 1979; Evolution of multiple genome mutations during long-term persistent infection by vesicular stomatitis virus. Cell 16:495–504
    [Google Scholar]
  10. Holland J., Spindler K., Horodyski F., Grabau E., Nichol S., Vandepol S. 1982; Rapid evolution of RNA genomes. Science 215:1577–1585
    [Google Scholar]
  11. Horodyski F. M., Nichol S. T., Spindler K., Holland J. 1983; Properties of DI particle resistant mutants of vesicular stomatitis virus isolated from persistent infections and undiluted passages. Cell 33:801–810
    [Google Scholar]
  12. Hovanec D. L., Air G. M. 1985; Antigenic structure of the hemagglutinin of influenza virus B/Hong Kong/8/73 as determined from gene sequence analysis of variants selected with monoclonal antibodies. Virology 139:384–392
    [Google Scholar]
  13. Ito H. Y., Ikuta S., Itakura K. 1982; Solid phase synthesis of polynucleotides. IV. Further studies on polystyrene copolymers for solid support. Nucleic Acids Research 10:1755–1769
    [Google Scholar]
  14. Jones C., Spindler K. R., Holland J. 1980; Studies on tumourigenicity of cells persistently infected with vesicular stomatitis virus in athymic nude mice. Virology 103:158–166
    [Google Scholar]
  15. Maxam A. M., Gilbert W. 1977; A new method for sequencing DNA. Proceedings of the National Academy of Sciences, U.S.A 74:560–564
    [Google Scholar]
  16. Minato N., Bloom B. R., Jones C., Holland J., Reid L. 1979; Mechanism of rejection of virus persistently infected tumor cells by athymic nude mice. Journal of Experimental Medicine 149:1117–1133
    [Google Scholar]
  17. Miyoshi K. R., Haung T., Itakura K. 1980; Solid phase synthesis of polynucleotides. IX. Usage of polystyrene resins for the synthesis of polydeoxyribonucleotides by the phosphotriester method. Nucleic Acids Research 8:5507–5517
    [Google Scholar]
  18. Moller J. R., Rager-Zisman B., Quan P., Schattner A., Panush A., Rose J. K., Bloom B. R. 1985; Natural killer cell recognition of target cells expressing different antigens of vesicular stomatitis virus. Proceedings of the National Academy of Sciences, U.S.A 82:2456–2459
    [Google Scholar]
  19. O’hara P. J., Nichol S. T., Horodyski F. M., Holland J. 1984a; Vesicular stomatitis virus defective interfering particles can contain extensive genomic sequence rearrangements and base substitutions. Cell 36:915–924
    [Google Scholar]
  20. O’hara P. J., Horodyski F. M., Nichol S. T., Holland J. 1984b; Vesicular stomatitis virus mutants resistant to defective interfering particles accumulate stable 5ʹ-terminal and fewer 3ʹ-terminal mutations in a stepwise manner. Journal of Virology 49:793–798
    [Google Scholar]
  21. Pringle C. R. 1970; Genetic characteristics of conditional lethal mutants of vesicular stomatitis virus induced by 5-fluorouracil, 5-azacytidine and ethylmethanesulfonate. Journal of Virology 5:559–567
    [Google Scholar]
  22. Reid L. M., Jones C. L., Holland J. 1979; Virus carrier state suppresses tumorigenicity of tumor cells in athymic (nude) mice. Journal of General Virology 42:609–614
    [Google Scholar]
  23. Rose J., Gallione C. J. 1981; Nucleotide sequences of the mRNAs encoding the vesicular stomatitis virus G and M proteins determined from cDNA clones containing the complete coding regions. Journal of Virology 39:519–528
    [Google Scholar]
  24. Rowlands D., Grabau E., Spindler K., Jones C., Semler B., Holland J. 1980; Virus protein changes and RNA termini alterations evolving during persistent infection. Cell 19:871–880
    [Google Scholar]
  25. Santoli D., Trinchieri G., Koprowski H. 1978; Cell mediated cytotoxicity against virus infected target cells in humans. II. Interferon induction and activation of natural killer cells. Journal of Immunology 121:532–538
    [Google Scholar]
  26. Schattner A., Rager-Zisman B., Bloom B. R. 1985; Persistent viral infection affects tumorigenicity of a neuroblastoma cell line. Cellular Immunology 90:103–114
    [Google Scholar]
  27. Seif I., Coulon P., Rollin P. E., Flamand A. 1985; Rabies virulence: effect on pathogenicity and sequence characterization of rabies virus mutations affecting antigenic site III of the glycoprotein. Journal of Virology 53:926–934
    [Google Scholar]
  28. Skehel J. J., Stevens D. J., Daniels R. S., Douglas A. R., Kuossow M., Wilson I. A., Wiley D. C. 1984; A carbohydrate side chain on hemagglutinins of Hong Kong influenza viruses inhibits recognition by a monoclonal antibody. Proceedings of the National Academy of Sciences, U.S.A 81:1779–1783
    [Google Scholar]
  29. Spindler K. R., Horodyski F. M., Holland J. 1982; High multiplicities of infection favor rapid and random evolution of vesicular stomatitis virus. Virology 119:96–108
    [Google Scholar]
  30. Welsh R. M., Hallenbeck L. A. 1980; Effect of virus infections on target cell susceptibility to natural killer cell-mediated lysis. Journal of Immunology 124:2491–2497
    [Google Scholar]
  31. Wiley D. C., Wilson I. A., Skehel J. J. 1981; Structural identification of the antibody-binding sites of Hong Kong influenza haemagglutinin and their involvement in antigenic variation. Nature, London 289:366–373
    [Google Scholar]
  32. Youngner J. S., Preble O. T., Jones E. V. 1978; Persistent infection of L cells with vesicular stomatitis virus: evolution of virus populations. Journal of Virology 28:6–13
    [Google Scholar]
  33. Youngner J. S., Jones E. V., Kelley M., Frielle D. W. 1981; Generation and amplification of temperature sensitive mutants during serial undiluted passage of versicular stomatitis virus. Virology 108:87–97
    [Google Scholar]
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