ABSTRACT
The virulence of herpes simplex virus (HSV) type 1 x type 2 intertypic recombinants was determined following infection of corneas of outbred New Zealand White rabbits. None of the four recombinants was as virulent for rabbits as type 1 parent. All the four recombinants having an insert of type 2 virus genome between 0.35 and 0.576 map units (m.u.) and/or 0.82 and 1.00 m.u. exhibited intermediate virulence between their type 1 and type 2 parents. The results indicate that intertypic recombinants are moderated in their virulence independent of their parental virulence and therefore there exists a multigenic control of HSV virulence.
Subject(s)
Animals , Genes, Viral , Herpes Simplex/etiology , Rabbits , Recombination, Genetic , Simplexvirus/classification , Virulence/geneticsABSTRACT
Using the rabbit eye model of latency, herpes simplex virus type 1 strain McKrae invariably reactivated after epinephrine iontophoresis, whereas type 2(HSV-2) virus strain HG 52 failed to reactivate. Both strains established a latent infection with the same frequency. To identify the viral genes involved in this reactivation difference, intertypic recombinants were selected following cotransfection of intact McKrae DNA and Xba I or Hpa I cleaved HG52 DNA. Eleven separately obtained recombinants containing HG52 inserts between 0.35-0.56 and/or 0.82-1.0 map units (mu) were isolated but as four that were tested reactivated with the same frequency as the parental Mckrae virus, it was established that the genes encoded between these map coordinates do not determine the reactivation difference.