1887

Abstract

SUMMARY

Infection of the lymphoblastoid CEM cell line with herpes simplex virus (HSV) type 1 results in a persistent infection with production of infectious virus. Evidence suggests that the persistent infection was not maintained by interferon or non-interferon-soluble antiviral inhibitors. Treatment of persistently infected cells with anti-HSV serum (termed CEM cells) or elevated temperature (39 °C) for 14 days (termed CEM cells) resulted in loss of evidence of virus. HSV DNA was not detected in CEM or CEM cells by Southern blot or hybridization. The CEM or CEM cells, however, were resistant to reinfection with homologous, parental virus (HSV), but were susceptible to heterologous virus (vesicular stomatitis virus). Resistance to reinfection with HSV was not absolute; CEM or CEM cells were less permissive to virus isolated from persistently infected cultures at times early in the course of infection, but were more permissive for HSV isolated at later times. Virus isolated later during persistent infection also displayed progressively increased virulence for the parental CEM cells. These results suggest that persistent infection of a human T lymphoblastoid cell line, CEM, with HSV-1 is maintained by a genetically determined cell-virus equilibrium, in which the resistance of cells and virulence of virus increase during persistence.

Keyword(s): HSV-1 , persistent infection and T cells
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1989-01-01
2022-01-27
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References

  1. Adams R. A., Flowers A., Sundeen R., Merk L. R. 1972; Chemotherapy and immune therapy of three human lymphomas serially transplantable in the neonatal Syrian hamster. Cancer 29:524–533
    [Google Scholar]
  2. Ahmed R., Canning W. M., Kauffman R. S., Sharpe A. H., Hallum J. V., Fields B. N. 1981; Role of the host Cell in persistent viral infection: coevolution of L cells and reovirus during persistent infection. Cell 25:325–332
    [Google Scholar]
  3. Armstrong J. A. 1971; Semi-micro, dye-binding assay for rabbit interferon. Applied Microbiology 21:723–725
    [Google Scholar]
  4. Blackmore R. V., Morgan H. R. 1967; Self-limiting infection with herpes simplex virus in cell culture. Acta virologica 11:1–12
    [Google Scholar]
  5. Buchman T. G., Simpson T., Nosal C., Roizman B. 1980; The structure of herpes simplex virus DNA and its application to molecular epidemiology. Annals of the New York Academy of Sciences 354:279–307
    [Google Scholar]
  6. Cummings P. J., Lakomy R. J., Rinaldo C. R. Jr 1981; Characterization of herpes simplex virus persistence in a human T lymphoblastoid cell line. Infection and Immunity 34:817–827
    [Google Scholar]
  7. Docherty J. I., O’Neill F. J., Rapp F. 1971; Differential susceptibility to herpes simplex viruses of hamster cell lines established after exposure to chemically inactivated herpesvirus. Journal of General Virology 13:377–384
    [Google Scholar]
  8. Eron K., Kosinski K., Hirsch M. S. 1976; Hepatitis in an adult caused by herpes simplex virus type 1. Gastroenterology 71:500–504
    [Google Scholar]
  9. Hammer S. M., Richter B. S., Hirsch M. S. 1981; Activation and suppression of herpes simplex virus in a human T lymphoid cell line. Journal of Immunology 111:144–148
    [Google Scholar]
  10. Hampar b., Burroughs M. A. K. 1969; Mechanisms of persistent herpes simplex virus infection in vitro. Journal of the National Cancer Institute 43:621–634
    [Google Scholar]
  11. Hay R., Macy M., Weinblatt A., Chen T. R. 1983; ATCC CCL 119 CCRF-CEM. American Type Collection Catalogue of Strains II80 Hatt H. D. Maryland; American Type Culture Collection:
    [Google Scholar]
  12. Kaplan J., Shope T. C., Peterson W. D. Jr 1974; Epstein-Barr virus negative human malignant T cell lines. Journal of Experimental Medicine 1391070–1076
    [Google Scholar]
  13. Locker H., Frenkel N. 1979; Bam HI, Kpn I, and Sal I restriction enzyme maps of the DNAs of herpes simplex virus strains Justin and F: occurrence of heterogeneities in defined regions of the viral DNA. Journal of Virology 32:429–441
    [Google Scholar]
  14. Maniatis T., Fritsch E. F., Sambrook J. 1982; Molecular Cloning: A Laboratory Manual. New York: Cold Spring Harbor Laboratory;
    [Google Scholar]
  15. Nilheden E., Jeansson S., Vahlne A. 1985a; Amplification of herpes simplex virus resistance in mouse neuroblastoma (C1300) cells. Archives of Virology 83:269–283
    [Google Scholar]
  16. Nilheden E., Jeansson S., Vahlne A. 1985b; Herpes simplex virus latency in a hyperresistant clone of mouse neuroblastoma (C1300) cells. Archives of Virology 83:319–325
    [Google Scholar]
  17. Post L. E., Conley A. J., Mocarski E. S., Roizman B. 1980; Cloning of reiterated and nonreiterated herpes simplex virus 1 sequences as Bam HI fragments. Proceedings of the National Academy of SciencesU.S.A 77:4201–12051
    [Google Scholar]
  18. Puga A., Cantin E. M., Notkins A. L. 1982; Homology between murine and human cellular DNA sequences and the terminal repetition of the S component of herpes simplex virus type 1 DNA. Cell 31:81–87
    [Google Scholar]
  19. Ramseur J. M., Friedman R. M. 1977; Prolonged infection of interferon-treated cells by vesicular stomatitis: possible role of temperature-sensitive mutants and interferon. Journal of General Virology 37:523–533
    [Google Scholar]
  20. Rinaldo C. R. Jr, Richter B. S., Black P. H., Callery R., Chess L., Hirsch M. 1978; Replication of herpes simplex virus and cytomegalovirus in human leukocytes. Journal of Immunology 120:130–136
    [Google Scholar]
  21. Rinaldo C. R. JR, Richter B. S., Black P. H., Hirsch M. S. 1979; Persistent infection of human lymphoid and myeloid cell lines with herpes simplex virus. Infection and Immunity 25:521–525
    [Google Scholar]
  22. Ron D., Tal J. 1985; Coevolution of cells and virus as a mechanism for the persistence of minute virus of mice in L-cells. Journal of Virology 55:424–430
    [Google Scholar]
  23. Schlief R. F., Wensink P. C. 1984; Isolating plasmid DNA. Practical Methods in Molecular Biology101–108 Manor Wien P. New York: Springer-Verlag;
    [Google Scholar]
  24. Tognon M., Cassai E., Rotola A., Roizman B. 1983; The heterogeneous regions in herpes simplex virus 1 DNA. Microbiologica 6:191–198
    [Google Scholar]
  25. Wiodahl B., Scheck A. C., Declercq E., Rapp F. 1982; High efficiency latency and activation of herpes simplex virus in human cells. Science 219:1145–1146
    [Google Scholar]
  26. Wigdahl B., Scheck A. C., Ziegler R. J., Declercq E., Rapp F. 1984; Analysis of the herpes simplex virus genome during in vitro latency in human diploid fibroblasts and rat sensory neurons. Journal of Virology 49:205–213
    [Google Scholar]
  27. Yamada A., Ttsurudome M., Hishiyama M., Ito Y. 1984; Abortive infection of mumps virus in murine cell lines. Journal of General Virology 65:973–980
    [Google Scholar]
  28. Youngner J. S., Preble O. T. 1980; Viral persistence: evolution of virus populations. Comprehensive Virology 1673–135 Fraenkel-Conrat H., Wagner R. R. New York: Plenum Press;
    [Google Scholar]
  29. Youssoufian H., Hammer S. M., Hirsch M. S., Mulder C. 1982; Methylation of the viral genome in an in vitro model of herpes simplex virus latency. Proceedings of the National Academy of SciencesU.S.A 79:2207–2210
    [Google Scholar]
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