1887

Abstract

SUMMARY

High multiplicity, undiluted passage of equine herpesvirus type 1 (EHV-1) in L-M cells resulted in the rapid production of virus particles whose genome was genetically less complex, contained more reiterated DNA sequences and exhibited a greater buoyant density (ρ = 1.724 g/ml) than the DNA (ρ = 1.716 g/ml) of standard virus. These data and the finding that these particles inhibited the replication of standard virus in interference assays confirmed that these were defective interfering (DI) particles (Henry ., 1979). Additional evidence for this has been obtained from the pattern of cyclic fluctuation in infectious virus titre through 17 serial passages as well as from the pronounced variation in the particle to plaque ratio for each passage. Total particle production was markedly reduced in cells infected with virus preparations containing DI particles and quantification of major cell-associated EHV-1 capsid species by electron microscopy and analysis in Renografin density gradients indicated that this reduction occurred at the level of capsid assembly. Although total capsid production was reduced in cells infected with DI particle preparations, the synthesis of I (immature) capsids increased relative to that of L (empty) capsids and these alterations in the assembly of capsid species could be related to changes in the synthesis of capsid proteins. In cells infected with EHV-1 preparations rich in DI particles, the synthesis of major capsid protein 150000 was greatly reduced, whereas core protein 46000, a major component of I capsids, was overproduced as compared to standard virus infection. Capsids produced in cells infected with virus preparations rich in DI particles were identical in polypeptide composition to those made in standard virus infection.

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1980-04-01
2022-01-18
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References

  1. Becker Y., Asher Y., Weinberg-Zahlering E., Rabkin S., Friedmann A., Kessler E. 1978; Defective herpes simplex virus DNA: circular and circular-linear molecules resembling rolling circles. Journal of General Virology 40:319–335
    [Google Scholar]
  2. Ben Porat T., Demarchi J. M., Kaplan A. S. 1974; Characterization of defective interfering viral particles present in a population of pseudorabies virions. Virology 60:29–37
    [Google Scholar]
  3. Ben Porat T., Louis B., Kaplan A. S. 1975; Further characterization for a population of defective interfering pseudorabies virions. Virology 65:179–186
    [Google Scholar]
  4. Bookout J., Hirsch I., Purifoy D. J. M., Biswal N. 1979; Herpes simplex virus types 1 and 2: comparison of the defective genomes and virus-specific polypeptides. Virology 93:598–604
    [Google Scholar]
  5. Campbell D. E., Kemp M. C., Perdue M. L., Randall C. C., Gentry G. A. 1976; Equine herpesvirus in vivo: cyclic production of a DNA density variant with repetitive sequences. Virology 69:737–750
    [Google Scholar]
  6. Courtney R. J., Benyesh-Melnick M. 1974; Isolation and characterization of a large molecular weight polypeptide of herpes simplex virus type 1. Virology 62:539–551
    [Google Scholar]
  7. Frenkel N., Jacob R. J., Honess R. W., Hayward G. S., Locker H., Roizman B. 1975; Anatomy of herpes simplex virus DNA III. Characterization of defective DNA molecules and biological properties of virus populations containing them. Journal of Virology 16:153–167
    [Google Scholar]
  8. Frenkel N., Locker H., Batterson W., Hayward G. S., Roizman B. F. 1976; Anatomy of herpes simplex virus DNA. VI. Defective DNA originates from the S. component. Journal of Virology 20:527–531
    [Google Scholar]
  9. Henry B. E., Newcomb W. W., O’Callaghan D. J. 1979; Biological and biochemical properties of defective interfering particles of equine herpesvirus type 1. Virology 92:495–506
    [Google Scholar]
  10. Huang A. S. 1973; Defective interfering viruses. Annual Review of Microbiology 27:101–117
    [Google Scholar]
  11. Huang A. S., Wagner R. R. 1966; Defective T particles of vesicular stomatitis virus. II. Biological role in homologous interference. Virology 30:173–181
    [Google Scholar]
  12. Kemp M. C., Perdue M. L., Rogers H. W., O’Call D. J., Randall C. C. 1974; Structural polypeptides of the hamster strain of equine herpes virus type 1: products associated with purification. Virology 61:361–375
    [Google Scholar]
  13. Laemmli U. K. 1970; Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature, London 227:680–684
    [Google Scholar]
  14. Lenard J., Compans R. W. 1975; Polypeptide composition of incomplete influenza virus grown in MDBK cells. Virology 62:418–426
    [Google Scholar]
  15. Murray B. K., Biswal N., Bookout J. B., Lanford R. E., Courtney R. J., Melnick J. L. 1975; Cyclic appearances of defective interfering particles of herpes simplex virus and the concomitant accumulation of early polypeptide VP 175. Intervirology 5:173–184
    [Google Scholar]
  16. O’Callaghan D. J., Randall C. C. 1976; Molecular anatomy of herpesviruses: recent studies. Progress in Medical Virology 22:152–210
    [Google Scholar]
  17. O’Callaghan D. J., Cheevers W. P., Gentry G. A., Randall C. C. 1968a; Kinetics of cellular and viral DNA synthesis in equine abortion (Herpes) virus-infection of L-M cells. Virology 36:104–114
    [Google Scholar]
  18. O’Callaghan D. J., Hyde J. M., Gentry G. A., Randall C. C. 1968b; Kinetics of viral deoxyribonucleic acid, protein and infectious particle production and alterations in host macromolecular synthesis in equine abortion (Herpes) virus-infected cells. Journal of Virology 2:793–804
    [Google Scholar]
  19. O’Callaghan D. J., Kemp M. C., Randall C. C. 1977; Properties of nucleocapsid species isolated from in vivo herpesvirus infection. Journal of General Virology 37:585–594
    [Google Scholar]
  20. O’Callaghan D. J., Allen G. P., Randall C. C. 1978; Structure and replication of the equine herpesviruses. In Equine Infectious Diseases vol IV pp 1–31 Edited by Bryans J., Gerber H. Princeton, New Jersey: Veterinary Publications Inc;
    [Google Scholar]
  21. O’Callaghan D. J., Henry B. E., Wharton J. H., Dauenhauer S. A., Vance R. B., Staczek J., Robinson R. A. 1980; Equine herpesviruses: biochemical studies on genomic structure, DI particles, oncogenic transformation, and persistent infection. In Herpesvirus DNA: Studies on the Internal Organization and Replication of the Viral Genome (in the press) Edited by Becker Y. The Hague: Nijhoff;
    [Google Scholar]
  22. Perdue M. L., Kemp M. C., Randall C. C., O’Callaghan D. J. 1974; Studies on the molecular anatomy of L-M cell strain of equine herpesvirus type I. Proteins of the nucleocapsids and intact virions. Virology 50:201–216
    [Google Scholar]
  23. Perdue M. L., Cohen J. C., Kemp M. C., Randall C. C., O’Callaghan D. J. 1975; Characterization of three species of nucleocapsids of equine herpesvirus type 1 (EHV-l). Virology 64:187–205
    [Google Scholar]
  24. Perdue M. L., Cohen J. C., Randall C. C., O’Callaghan D. J. 1976; Biochemical studies of the maturation of herpesvirus nucleocapsid species. Virology 74:194–208
    [Google Scholar]
  25. Robinson R. A., Henry B. E., Duff R. G., O’Callaghan D. J. 1980; Oncogenic transformation by equine herpesvirus (EHV). 1. Properties of hamster embryo cells transformed by ultraviolet-irradiated EHV-1. Virology 101: (in the press)
    [Google Scholar]
  26. Schaffer P. A., Aron G. M., Biswal N., Benyesh-Melnick M. 1973; Temperature-sensitive mutants of herpes simplex virus type i: isolation, complementation and partial characterization. Virology 52:57–71
    [Google Scholar]
  27. Soehner R. L., Gentry G. A., Randall C. C. 1965; Some physicochemical characteristics of equine abortion virus nucleic acid. Virology 26:395–404
    [Google Scholar]
  28. Stegmann B., Zentgraf H., Ott A., Schroder C. H. 1978; Synthesis and packaging of herpes simplex virus DNA in the course of virus passages at high multiplicity. Intervirology io:228–240
    [Google Scholar]
  29. Vance R. B., Robinson R. A., Henry B. E., O′Callaghan D. J. 1978; sHerpesvirus oncogenesis and persistent infection: model systems using inactivated virus and defective interfering (DI) particles. Clinical Research 26:777
    [Google Scholar]
  30. Wagner J., Skare J., Summers W. C. 1975; Analysis of DNA of defective herpes simplex virus type 1 by restriction endonuclease cleavage and nucleic acid hybridization. Cold Spring Harbor Symposium on Quantitative Biology 39:683–685
    [Google Scholar]
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