Latency competence of herpes simplex virus strains ANG, ANGpath and its gC and gE minus mutans

The latency competence of herpes simplex virus type 1 (HSV-1) strains SC16, KOS, ANG, ANGpath and its mutants ANGpathgC18 (gC minus, spontaneous point mutation), KOSgC39 (gC minus deletion), ANGpathI2-4 (gE minus deletion), and ANGpathgCI-8 (gE and gC minus double mutan) was compared and DBA/2 mice. While the latent SC16 and KOS reactivated spontaneously in explanted homolateral trigeminal ganglion fragments coming from Velaz DBA/2 mice, methylation inhibitor 5-azacytidine (5-AzaC) was required to achieve reactivation of SC16 in the ganglion explants from Hannover DBA/2 mice. Reactivation of ANGpath in the cultured trigeminal ganglia from both lines of DBA/2 mice occurred only in the presence of the drug. The compound also enhanced the reactivation incidence in the ganglion explants from ANG-infected Hannover DBA/2 mice but not from Velaz DBA/2 mice: in the latter it remained low even in the presence of the inducer. Both gE- mutants failed to establish latency as judged by the failure of reactivation either in the presence or the absence of 5-AzaC. This seemed in accordance with the absence of neural (quick axonal) spread of these mutans in mice (Rajcáni et al., 1990). In contrast, both gC- mutans established latency: ANGpathgC18 at an unchanged rate and KOSgC39 at a lower frequency than the parent strain.