1887

Abstract

Summary

A model of herpes simplex virus type 2 (HSV-2) infection was developed in the guinea-pig that permits investigation of the role of neural spread of virus in the pathogenesis of genital skin disease. After HSV-2 inoculation of an abraded area lateral to the external genital skin, virus was first detected in the ipsilateral (to the inoculation site) peripheral nerves or genital skin on day 2 or 3 post-inoculation followed by detection in the ipsilateral dorsal root ganglia and spinal cord on day 3 or 4. Virus also spread to the contralateral dorsal root ganglia, contralateral peripheral nerves and contralateral genital skin on day 4 or 5 although lesions were only rarely detected on the contralateral side. Genital skin lesions first developed on day 5 and were followed by the development of lesions along the medial aspect of the ipsilateral hindlimb. Virus was first detected in the vaginal vault on day 4 or 5. The development of lesions appeared to be unrelated to vaginal virus replication but was associated with the recovery of virus from peripheral nerves. Recurrent genital skin lesions were seen more commonly on the inoculated side than the contralateral side. Since the development of skin lesions appeared to result from virus emerging from nerve endings, an event similar to the terminal event that is believed to be involved in the development of recurrent lesions, we now have a model which may be useful in further exploring the pathogenesis of herpetic disease.

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/content/journal/jgv/10.1099/0022-1317-67-9-1851
1986-09-01
2024-10-05
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References

  1. Bernstein D. I., Stanberry L. R., Harrison C. J., Kappes J. C., Myers M. G. 1986; Antibody response, recurrence patterns and subsequent herpes simplex virus type 2 (HSV-2) re-infection following initial HSV-2 infection of guinea-pigs: effects of acyclovir. Journal of General Virology 67:1601–1612
    [Google Scholar]
  2. Blyth W. A., Harbour D. A., Hill T. J. 1984; Pathogenesis of zosteriform spread of herpes simplex virus in the mouse. Journal of General Virology 65:1477–1486
    [Google Scholar]
  3. Bryson Y. J., Dillon M., Lovett M., Acuna G., Taylor S., Cherry J. D., Johnson B. L., Wiesmer E., Growdon W., Creagh-Kirk T., Kenney R. 1983a; Treatment of first episodes of genital herpes simplex virus infection with oral acyclovir. New England Journal of Medicine 308:916–921
    [Google Scholar]
  4. Bryson Y., Dillon M., Lovett M., Bernstein D. I., Sayre J. 1983b; A prospective long term study of the natural history of genital HSV infections. In Program and Abstracts, 23rd Interscience Conference on Antimicrobial Agents and Chemotherapy (Las Vegas) abstract no. 739
    [Google Scholar]
  5. Gerdes J. C., Smith D. S. 1983; Recurrence phenotypes and establishment of latency following rabbit keratitis produced by multiple herpes simplex virus strains. Journal of General Virology 64:2441–2454
    [Google Scholar]
  6. Klein R. J., Destefano E. 1983; Dissemination of herpes simplex virus in ganglia after footpad inoculation in neurectomized and non-neurectomized mice. Archives of Virology 77:231–238
    [Google Scholar]
  7. Lycke E., Kristensson K., Svennerholm B., Vahlne A., Ziegler R. 1984; Uptake and transport of herpes simplex virus in neurites of rat dorsal root ganglia cells in culture. Journal of General Virology 65:55–64
    [Google Scholar]
  8. Openshaw H., Ellis W. G. 1983; Herpes simplex virus infection of motor neurons: hypoglossal model. Infection and Immunity 42:409–413
    [Google Scholar]
  9. Price R. W., Katz B. J., Notkins A. L. 1975; Latent infection of the peripheral ANS with herpes simplex virus. Nature, London 257:686–687
    [Google Scholar]
  10. Scriba M. 1976; Recurrent genital herpes simplex virus (HSV) infection of guinea pigs. Medical Microbiology and Immunology 162:201–208
    [Google Scholar]
  11. Scriba M., Tatzber F. 1981; Pathogenesis of herpes simplex virus infections in guinea pigs. Infection and Immunity 34:655–661
    [Google Scholar]
  12. Simmons A., Nash A. A. 1984; Zosteriform spread of herpes simplex virus as a model of recrudescence and its use to investigate the role of immune cells in prevention of recurrent disease. Journal of Virology 52:816–821
    [Google Scholar]
  13. Simmons A., Nash A. A. 1985a; Role of antibody in primary and recurrent herpes simplex virus infection. Journal of Virology 53:944–948
    [Google Scholar]
  14. Simmons A., Nash A. A. 1985b; Innate resistance to HSV infection of the nervous system involves genes of the MHC. Abstracts, Herpesvirus Workshop (Ann Arbor, Michigan) no. 225
    [Google Scholar]
  15. Stanberry L. R., Kern E. R., Richards J. T., Abbott T. M., Overall J. C. Jr 1982; Genital herpes in guinea pigs: pathogenesis of the primary infection and description of recurrent disease. Journal of Infectious Diseases 146:397–404
    [Google Scholar]
  16. Stanberry L. R., Kit S., Myers M.G. 1985; Thymidine kinase deficient herpes simplex virus type 2 genital infection in guinea pigs. Journal of Virology 55:322–328
    [Google Scholar]
  17. Tullo A. B., Shimeld C., Blyth W. A., Hill T. J., Easty D. L. 1982; Spread of virus and distribution of latent infection following ocular herpes simplex in the non-immune mouse. Journal of General Virology 6395–101
    [Google Scholar]
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