Spread of HSV and establishment of latency after corneal infection in inbred XXXX .

@entity778 @entity2194 @entity1034 @entity1036 @entity19 @entity14985 @entity2343 @entity7840
The @entity778 (HSV) through neural tissues was studied in three inbred @entity19 strains that differ in susceptibility to @entity1034 . The left eyes of BALB/c, C57BL/6, and DBA/2 @entity19 were inoculated topically with @entity778 . The optic and trigeminal nerves, trigeminal ganglia, and eyes were assayed for infectious @entity778 on days 1, 2, 3, 4, 7, 9, 11 and 14 after inoculation. At 2-4 months post-inoculation, eyes and trigeminal ganglia were assayed for latent @entity778 . Up to 7 days post-inoculation, infectious @entity778 was present at a similar frequency in the inoculated eyes of @entity19 from all three strains. The quantity of @entity778 recovered, however, was @entity19 -dependent: DBA @entity19 yielded the most @entity778 ; C57BL/6, the least. The frequency of @entity778 recovery and the quantity of @entity778 recovered from trigeminal nerves and ganglia also varied according to @entity19 . @entity778 was recovered from the uninoculated right eye of some @entity7840 and C57BL/6 @entity19 1 wk after inoculation. The overall incidence of latency differed among inbred @entity19 strains. However, in @entity19 that developed @entity2194 ( @entity14985 , @entity2343 , or @entity1036 ), there was no host strain-related difference in the incidence of latency. These results support the hypothesis that host genetic factors play a role in controlling HSV replication and the spread of @entity778 to neural tissues after ocular HSV inoculation. This control may influence the development and severity of disease. However, once infection occurs, latency is established in both susceptible and resistant @entity19 strains.
