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The pathogenicity of thymidine kinase-deficient mutants of herpes simplex virus in mice

  • H. J. Field (a1) and P. Wildy (a1)

The pathogenicity for mice of two mutants of herpes simplex virus (type 1 and type 2), which fail to induce thymidine kinase, were compared with their respective parent strains. The mutants were much less virulent than the parents following either intracerebral or peripheral inoculation. The replication of the virus at the site of inoculation and its progression into the nervous system were studied. Following a very large inoculum in the ear, the type 1 mutant was found to establish a latent infection in the cervical dorsal root ganglia. Mice inoculated intracerebrally with small doses of the mutant viruses were solidly immune to challenge with lethal doses of the parent strain.

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H. J. Field & T. J. Hill (1974). The pathogenesis of pseudorabies in mice following peripheral inoculation. Journal of General Virology 23, 145–57.

T. J. Hill , H. J. Field & W. A. Blyth (1975). Acute and recurrent infection with herpes simplex virus in the mouse: a model for studying latency and recurrent disease. Journal of General Virology 28, 341–53.

A. T. Jamieson , G. A. Gentry & J. H. Subak-Sharpe (1974). Induction of both thymidine and deoxycytidine kinase activity by herpes viruses. Journal of General Virology 24, 465–80.

M. E. Thouless (1972). Serological properties ofthymidine kinase produced in cells infected with type 1 or type 2 herpes virus. Journal of General Virology 17, 307–15.

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Epidemiology & Infection
  • ISSN: 0950-2688
  • EISSN: 1469-4409
  • URL: /core/journals/epidemiology-and-infection
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