PURPOSE. To identify possible neuronal pathways leading to herpetic ocular
disease after primary oral infection in mice.
METHODS. The SC16 strain of herpes simplex virus (HSV)-1 (10(6) plaque-form
ing units) was injected into the mucocutaneous border of the left upper lip
. Animals were killed 2 to 10 days postinoculation (DPI). Spread of the vir
us in neural structures was studied by immunochemistry.
RESULTS. HSV1 first replicated at the site of inoculation and then at the s
uperior cervical ganglion (at 2 DPI). The trigeminal ganglion and the facia
l nerve fibers were infected by 4 DPI. Infection of the ciliary body and ir
is occurred at 6 DPI, together with several brain stem nuclei belonging to
the autonomic or sensory pathways. Between 8 and 10 DPI, the neural infecti
on gradually cleared up, except for the ipsilateral sympathetic ganglion, a
nd ipsilateral keratitis appeared in some animals.
CONCLUSIONS. The pattern of viral dissemination in this mouse model suggest
s that infection of iris and ciliary body results from transfer of virus in
the superior cervical ganglion from sympathetic neurons innervating the li
p to neighboring neurons innervating the anterior uvea. Later, zosteriform
spread of virus from the trigeminal system may have contributed to the clin
ical and histologic findings.