1887

Abstract

SUMMARY

A rabies virus persistent infection in BHK21 S13 cells was established and maintained in culture for more than 4 years. Initially, the cultures produced a large plaque virus similar to that produced by the original virus, but between the 10th and 20th passage, this was replaced by a small plaque variant. By the 200th passage, infectious virus could no longer be detected in the medium. After further cell passages (⩾ 300) no infectious particles could be detected in the medium. At various passage levels, the persistently infected cells were labelled with [S]methionine and the virus antigens immunoprecipitated and analysed by polyacrylamide gel electrophoresis. No changes in the virus polypeptides were observed in the establishment of the persistent state. However, after the 20th passage (predominance of small plaque variant) there was an increase in the size of the glycoprotein. This was followed (164th passage) by a change in the M1 polypeptide which was subsequently further modified in the defective state (⩾ 300 passages). Virus isolated from the 400th passage by treatment of the cells with DEAE-dextran, was also modified in the glycoprotein and M1 polypeptides and contained less L polypeptide than the original virus. This virus grew more slowly, to a lower titre and was no longer pathogenic in suckling mice.

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/content/journal/jgv/10.1099/0022-1317-57-1-169
1981-11-01
2022-01-23
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References

  1. Andzhaparidze O. G., Bogomolova N. N., Boriskin Y. S., Bektemirova M. S., Drynov I. D. 1981; Comparative study of rabies virus persistence in human and hamster cell lines. Journal of Virology 37:1–6
    [Google Scholar]
  2. Bijlenga G., Joubert L. 1980; Seroneutralisation antirabique chez le chat. Comparaison entre deux methodes ‘in vitro’: plages et immunofluorescence rapide, inoculation a la souris. Bulletin du Societaire de Science Veterinaire et Medecine Comparee, Lyon 82:293–297
    [Google Scholar]
  3. Bonner M. W., Laskey R. A. 1974; A film detection method for tritium-labelled protein and nucleic acid in polyacrylamide gels. European Journal of Biochemistry 46:83–88
    [Google Scholar]
  4. Fernandes M. V., Wiktor T. J., Koprowski H. 1964; Endosymbiotic relationship between animal viruses and host cells. Journal of Experimental Medicine 120:1099–1118
    [Google Scholar]
  5. Fisher L. E., Eapp F. 1979; Role of virus variants and cells in maintenance of persistent infection by measles virus. Journal of Virology 30:64–68
    [Google Scholar]
  6. Giraudon P., Wild T. F. 1981; Monoclonal antibody against measles virus. Journal of General Virology 54:325–332
    [Google Scholar]
  7. 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 of the United States of America 71:2956–2960
    [Google Scholar]
  8. Holland J. J., Villarreal L. P., Breindl M. 1976; Factors involved in the generation and the replication of rhabdovirus defective T particles. Journal of Virology 17:805–815
    [Google Scholar]
  9. Holland J. J., Grabau E. A., Jones C. L., Semler B. L. 1979; Evolution of multiple genome mutations during long-term persistent infections by vesicular stomatitis virus. Cell 16:495–504
    [Google Scholar]
  10. Huang A. S., Baltimore D. 1970; Defective viral particles and viral disease processes. Nature, London 226:325–327
    [Google Scholar]
  11. Kawai A. 1977; Transcriptase activity associated with rabies virion. Journal of Virology 24:826–835
    [Google Scholar]
  12. Kawai A., Matsumoto S., Tanabe K. 1975; Characterisation of rabies viruses recovered from persistently infected BHK cells. Virology 67:520–533
    [Google Scholar]
  13. Laemmli U. K. 1970; Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature, London 227:680–685
    [Google Scholar]
  14. Meinkoth J., Kennedy S. I. T. 1980; Semliki Forest virus persistence in mouse L929 cells. Virology 100:141–155
    [Google Scholar]
  15. Neurath A. R., Vernon S. K., Dobkin M. B., Rubin B. A. 1972; Characterisation of subviral components resulting from treatment of rabies virus with tri (n-butyl) phosphate. Journal of General Virology 14:33–48
    [Google Scholar]
  16. Nishiyama Y. 1977; Studies of L cells persistently infected with VSV: factors involved in the regulation of persistent infection. Journal of General Virology 35:265–279
    [Google Scholar]
  17. Pontecorvo G. 1975; Production of mammalian somatic cell hybrids by means of polyethylene-glycol treatment. Somatic Cell Genetics 1:397–400
    [Google Scholar]
  18. Preble O. T., Youngner J. S. 1975; Temperature sensitive viruses and the etiology of chronic and inapparent infections. Journal of Infectious Diseases 131:467–473
    [Google Scholar]
  19. Ramseur J. M., Friedman R. M. 1977; Prolonged infection of interferon-treated cells by vesicular stomatitis virus: possible role of temperature-sensitive mutants and interferon. Journal of General Virology 37:523–533
    [Google Scholar]
  20. 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]
  21. Sokol F., Stancek D., Koprowski H. 1971; Structural proteins of rabies virus. Journal of Virology 1:241–249
    [Google Scholar]
  22. Wechsler S. L., Rustigan R., Stallcup K. C., Byers K. B., Winston S. H., Fields B. N. 1979; Measles virus-specified polypeptide synthesis in two persistently infected HeLa cell lines. Journal of Virology 31:677–684
    [Google Scholar]
  23. Wiktor T. J., Clark H. F. 1972; Chronic rabies virus infection of cell cultures. Infection and Immunity 6:988–995
    [Google Scholar]
  24. Wild T. F., Dugre R. 1978; Establishment and characterization of a subacute sclerosing panencephalitis (measles) virus persistent infection in BGM cells. Journal of General Virology 38:113–124
    [Google Scholar]
  25. Wild T. F., Greenland T. 1979; A study of the measles virus-induced proteins incorporated into the cell membrane. Intervirology 11:275–281
    [Google Scholar]
  26. Wild T. F., Bernard A., Greenland T. 1981; Measles virus: evolution of a persistent infection in BGM cells. Archives of Virology 61:297–308
    [Google Scholar]
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