Medical Microbiology and Immunology

, Volume 175, Issue 5, pp 281–292 | Cite as

Pathogenesis of genital herpes simplex virus infection in mice

IV. Quantitative aspects of viral latency
  • A. -M. Eis
  • K. E. Schneweis
Article

Abstract

Experiments in the mouse model of herpes simplex virus (HSV) infection involving the intact genital mucous membranes as inoculation site yielded the following results. In untreated mice the extent of latency was correlated with the degree of peripheral virus replication. This correlation could not be observed when the course of infection was interrupted by chemotherapy, interferon, or passive immunization. Acyclovir had little effect on peripheral virus multiplication, but markedly reduced latent ganglionic infection. As acute ganglionic infection and virus concentration in the spinal nerves were already reduced, acyclovir is assumed to inhibit either virus penetration into the nerve endings or virus replication in the ganglia. Interferon apparently has an active role in the elimination of virus infected cells from the ganglia, as its effect was restricted to a reduced rate of latency and of lethality. Passive immunization with antiserum led to similar results as ACV-treatment. While lacking a pronounced effect on virus replication in the mucous membranes, specific antibody was found to influence both virus elimination from the ganglia, and conversion from productive to latent ganglionic infection. Immune lymphocytes proved to be the only agent capable of suppressing peripheral infection, thereby inhibiting the neural spread of the virus. These results suggest that the decrease in latency may result from modulations occurring at different stages in the course of infection.

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References

  1. 1.
    Cook ML, Stevens JG (1983) Restricted replication of herpes simplex virus in spinal ganglia of resistant mice is accompanied by an early infiltration of immunoglobulin G-bearing cells. Infect Immun 40:752–758PubMedGoogle Scholar
  2. 2.
    Davis WB, Taylor JA, Oakes JE (1979) Ocular infection with herpes simplex virus type 1: Prevention of acute herpetic encephalitis by systemic administration of virus-specific antibody. J Infect Dis 140:534–540PubMedGoogle Scholar
  3. 3.
    Finter NB (1965) A comparison of the amounts of mouse interferon obtained from different sources. Nature 206:597–599PubMedGoogle Scholar
  4. 4.
    Harbour DA, Hill TJ, Blyth WA (1981) Acute and recurrent herpes simplex in several strains of mice. J Gen Virol 55:31–40PubMedGoogle Scholar
  5. 5.
    Kapoor AK, Nash AA, Wildy P (1982) Pathogenesis of herpes simplex virus in B cell-suppressed mice: The relative roles of cell-mediated and humoral immunity. J Gen Virol 61:127–131PubMedGoogle Scholar
  6. 6.
    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. J Gen Virol 65:55–64PubMedGoogle Scholar
  7. 7.
    Myers M, Glasgow LA, Galasso GI (1982) Herpes workshop. National Institutes of Allergy and Infectious Disease. J Infect Dis 145:774–782PubMedGoogle Scholar
  8. 8.
    Oakes JE, Rosemond-Hornbeak H (1978) Antibody-mediated recovery from subcutaneous herpes simplex virus type 2 infection. Infect Immun 21:489–495PubMedGoogle Scholar
  9. 9.
    Reed JL, Muench H (1938) A simple method for estimating fifty percent endpoints. Amer J Hyg 27:493–497Google Scholar
  10. 10.
    Schneweis KE, Gruber J, Hilfenhaus J, Möslein A, Kayser M, Wolff MH (1981) The influence of different modes of immunization on the experimental genital herpes simplex virus infection of mice. Med Microbiol Immunol 169:269–279PubMedGoogle Scholar
  11. 11.
    Schneweis KE, Olbrich M, Saftig V, Scholz R (1982) Effects of genetic resistance against herpes simplex virus in vaginally infected mice. Med Microbiol Immunol 171:161–169PubMedGoogle Scholar
  12. 12.
    Schneweis KE, Forstbauer H, Olbrich M, Tag M (1984) Pathogenesis of genital herpes simplex virus infection in mice: III. Comparison of the virulence of wild and mutant strains. Med Microbiol Immunol 173:187–196CrossRefPubMedGoogle Scholar
  13. 13.
    Sethi KK, Brandis H (1980) The role of vesicular stomatitis virus major glycoprotein in determining the specificity of virus-specific and H-2-restricted cytolytic T cells. Eur J Immunol 10:268–272PubMedGoogle Scholar
  14. 14.
    Sethi KK, Omata Y, Schneweis KE (1983) Protection of mice from fatal herpes simplex virus type 1 infection by adoptive transfer of cloned virus-specific and H-2-restricted cytotoxic T lymphocytes. J Gen Virol 64:443–447PubMedGoogle Scholar
  15. 15.
    Stevens JC, Cook ML (1971) Latent herpes simplex virus in spinal ganglia of mice. Science 173:843–845PubMedGoogle Scholar
  16. 16.
    Stevens JC, Cook ML (1973) Pathogenesis of herpetic neuritis and ganglionitis in mice: Evidence for intra-axonal transport of infection. Infect Immun 7:272–288PubMedGoogle Scholar
  17. 17.
    Stewart II WE (1979) The interferon system. Springer-Verlag, ViennaGoogle Scholar
  18. 18.
    Sturn B, Schneweis KE (1978) Protective effect of an oral infection with herpes simplex virus type 2. Med Microbiol Immunol 165:119–127PubMedGoogle Scholar
  19. 19.
    Wildy P, Gell PGH (1985) The host response to herpes simplex virus. Brit Med Bull 41:86–91PubMedGoogle Scholar

Copyright information

© Springer-Verlag 1986

Authors and Affiliations

  • A. -M. Eis
    • 1
  • K. E. Schneweis
    • 1
  1. 1.Institute of Medical Microbiology and ImmunologyUniversity of BonnBonn 1Federal Republic of Germany

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