1887

Abstract

SUMMARY

preinfection of chicks with rabies virus (RV) or vesicular stomatitis virus (VSV) 1026 inhibits tumour formation after superinfection with Rous sarcoma virus (RSV). The degree of inhibition depends on the titre of the infecting viruses and the interval between rhabdovirus and RSV infection. , cells preinfected with VSV 1026 under non-permissive conditions and superinfected with RSV, are not transformed as judged by cell morphology, serum requirement for growth or the capacity to form colonies in soft agar, all these being the same as in uninfected cells. Doubly infected cells take up less deoxyglucose than cells infected with RSV only and more than cells infected with VSV only. RSV multiplication is inhibited in doubly infected cells: the supernatant fluid of these cells contains fewer focus-forming units and less reverse transcriptase activity than that of cells infected with RSV only. Doubly infected cells contain both VSV and RSV internal antigens 15 days after infection. The supernatant fluid of cells infected with VSV and maintained under non-permissive conditions inhibits transformation by RSV and multiplication of RSV, but not of VSV. Under non-permissive conditions, the rhabdoviruses undergo at least part of the infectious cycle, but no infectious virus is produced. RV antigen can be detected in the brain of parenterally infected chicks and VSV antigen in cells infected 15 days previously. We conclude that the inhibition of RSV multiplication and expression is probably due to one or more processes linked to the persistence of rhabdovirus components and that it cannot be attributed exclusively to interferon.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-64-2-275
1983-02-01
2021-10-27
Loading full text...

Full text loading...

/deliver/fulltext/jgv/64/2/JV0640020275.html?itemId=/content/journal/jgv/10.1099/0022-1317-64-2-275&mimeType=html&fmt=ahah

References

  1. Carver D. H., Marcus P. I. 1967; Enhanced interferon production from chick embryo cells aged in vitro. Virology 32:247–257
    [Google Scholar]
  2. Chen C. Y., Crouch N. A. 1978; Shope fibroma induced facilitation of vesicular stomatitis virus adsorption and replication in non-permissive cells. Virology 85:43–62
    [Google Scholar]
  3. Ehrenfeld E., Lund H. 1977; Untranslated vesicular stomatitis virus messenger RNA after poliovirus infection. Virology 106:297–308
    [Google Scholar]
  4. Francoeur A. M., Lam T., Stanners C. P. 1980; PIF, a highly sensitive plaque assay for the induction of interferon. Virology 106:526–536
    [Google Scholar]
  5. Hamilton D. H., Moyer R. W., Moyer S. A. 1980; Characterization of the non-permissive infection of rabbit cornea cells by vesicular stomatitis virus. Journal of General Virology 49:273–287
    [Google Scholar]
  6. Hatanaka M., Hanafusa H. 1970; Analysis of a functional change in membrane in the process of transformation by Rous sarcoma virus; alterations in the characteristics of sugar transport. Virology 41:647–652
    [Google Scholar]
  7. Kravchenko A. T., Altstein A. D., Voronin E. S. 1965; Interference between influenza and Rous sarcoma viruses in chicks. Acta virologica 9:130–136
    [Google Scholar]
  8. Kravchenko A. T., Voronin E. S., Kosmiadi G. A. 1967; Effects of antirabies vaccine and fixed rabies virus on the development of tumours caused by Rous sarcoma virus. Acta virologica 11:145–149
    [Google Scholar]
  9. Little S. P., Huang A. S. 1978; Shedding of glycoportein from vesicular stomatitis virus-infected cells. Journal of Virology 27:330–339
    [Google Scholar]
  10. McPherson L., Montagnier L. 1964; Agar suspension culture for the selective assay of cells transformed by polyoma virus. Virology 23:327–333
    [Google Scholar]
  11. Mcsharry J., Choppin P. W. 1978; Biological properties of the VSV glycoprotein. I. Effects of the isolated glycoprotein on host macromolecular synthesis. Virology 84:172–182
    [Google Scholar]
  12. Marcus P. L. 1979; The interferon system and rhabdoviruses. In Rhabdoviruses vol 3: pp 2–12 Edited by Bishop D. H. L. Boca Raton, Fla.: CRC Press;
    [Google Scholar]
  13. Marcus P. I., Sekellick M. J. 1974; Cell killing by viruses. I. Comparison of cell-killing, plaque-forming and defective interfering particles of vesicular stomatitis virus. Virology 57:321–338
    [Google Scholar]
  14. Mouttet M. E., Bechet J. M., Montagnier L. 1980; Enhanced replication of herpes simplex virus type 1 in BHK cells transformed by hamster sarcoma virus. Intervirology 14:78–83
    [Google Scholar]
  15. Nishiyama Y. 1977; Studies of L cells persistently infected with VSV: factors involved in the regulation of persisted infection. Journal of General Virology 35:265–279
    [Google Scholar]
  16. Otto M. J., Lenard J. L. 1980; The influence of the host cell on the inhibition of virus protein synthesis in cells doubly infected with vesicular stomatitis virus and Mengo virus. Journal of General Virology 50:293–307
    [Google Scholar]
  17. Rao S. M., Shirodkar M. V. N. 1978; Rous sarcoma virus blockage by rabies virus strains and rabies-induced plasma factor. Indian Journal of Medical Research 68:717–723
    [Google Scholar]
  18. Ross J., Scolnick E. M., Aaronson S. A., Todaro O. J. 1971; Separation of murine cellular and murine leukemia virus DNA polymerases. Nature New Biology 231:163–167
    [Google Scholar]
  19. Saxton R. E., Stevens J. G. 1972; Restriction of herpes simplex replication by poliovirus. A selective inhibition of viral translation. Virology 48:207–220
    [Google Scholar]
  20. Sekellick M. J., Marcus P. I. 1979; Persistent infections by rhabdoviruses. In Rhabdoviruses vol 3: pp 68–97 Edited by Bishop D. H. L. Boca Raton, Fla.: CRC Press;
    [Google Scholar]
  21. Seligman E. B. Jr 1973; Laboratory techniques in rabies. In WHO Monograph no. 23 pp 279–280 Edited by Kaplan M., Koprowski H. Geneva: World Health Organization;
    [Google Scholar]
  22. Stanners C. P., Francoeur A. M., Lam T. 1977; Analysis of a VSV mutant with attenuated cytopathogenicity: mutation in viral function P for inhibition of protein synthesis. Cell 11:273–281
    [Google Scholar]
  23. Stewart W. E. II 1979 The Interferon System pp 144:269–302 Wien & New York: Springer-Verlag;
    [Google Scholar]
  24. Tannenbaum J., Goorha R., Granoff A. 1978; Inhibition of vesicular stomatitis virus replication by frog virus 3: selective action on secondary transcription. Virology 89:560–569
    [Google Scholar]
  25. Temin H. M., Rubin H. 1958; Characteristics of an assay for Rous sarcoma virus and Rous sarcoma cells in tissue culture. Virology 6:669–688
    [Google Scholar]
  26. Thacore T. R., Youngner J. S. 1975; Abortive infection of a rabbit cornea cell line by vesicular stomatitis virus; conversion to productive infection with vaccinia virus. Journal of Virology 16:322–329
    [Google Scholar]
  27. Weiss R. A., Boettiger D., Murphy H. M. 1977; Pseudotypes of avian sarcoma viruses with envelope properties of vesicular stomatitis virus. Virology 76:808–825
    [Google Scholar]
  28. Winship T. R., Thacore H. R. 1979; Inhibition of vesicular stomatitis virus-defective interfering particle synthesis by Shope fibroma virus. Virology 93:515–526
    [Google Scholar]
  29. Zajac B. A., Hummeler K. 1970; Morphogenesis of the nucleoprotein of vesicular stomatitis virus. Journal of Virology 6:243–252
    [Google Scholar]
http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-64-2-275
Loading
/content/journal/jgv/10.1099/0022-1317-64-2-275
Loading

Data & Media loading...

Most cited this month Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error