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Biological basis for virulence of three strains of herpes simplex virus type 1

F Sedarati1, J G Stevens

  • 1Department of Microbiology and Immunology, UCLA School of Medicine 90024.

The Journal of General Virology
|September 1, 1987
PubMed

Insights

Herpes simplex virus type 1 (HSV-1) strains F, HF, and HFEM show reduced virulence in mice due to replication defects. These HSV-1 strains can still cause lethal infections when interacting within the animal.

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Herpes simplex virus type 1 (HSV-1) causes various infections.
  • Understanding HSV-1 strain pathogenicity is crucial for developing effective treatments.
  • Virulence factors and host cell interactions dictate HSV-1 disease progression.

Purpose of the Study:

  • To compare the pathogenicity and growth characteristics of HSV-1 strains F, HF, and HFEM with neurovirulent strains.
  • To investigate the replication deficiencies and genetic complementation of attenuated HSV-1 strains.
  • To elucidate the mechanisms underlying HSV-1 avirulence and potential for lethal infections.

Main Methods:

  • Pathogenicity testing in mouse models (intracranial and footpad inoculation).
  • In vitro and in vivo growth characteristic analysis.
  • Genetic complementation assays to assess viral interactions and genotypes.

Main Results:

  • HSV-1 strains F, HF, and HFEM exhibited reduced virulence in mouse brains and were avirulent after peripheral inoculation.
  • These strains showed high thymidine kinase activity but had general replication deficiencies in mouse cells.
  • Replication restriction was cell-specific for strains F and HF in murine cells, while HFEM replicated poorly in all tested cell types.
  • Genetic complementation revealed distinct genotypes among F, HF, and HFEM, with strain F complementing the other two.
  • Co-infection with highly restricted HSV-1 strains (F and HF) could lead to lethal infections in animals.

Conclusions:

  • HSV-1 strains F, HF, and HFEM possess distinct genetic determinants for avirulence and replication deficiency.
  • Despite replication defects, these strains can interact and cause severe disease, highlighting complex viral interplay.
  • Further research into HSV-1 attenuation mechanisms and viral interactions is warranted for therapeutic strategies.

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