Primary infection with HSV-1 occurs following inoculation of mucosal or skin surfaces by direct contact. Most ocular disease is thought to represent recurrent HSV disease following the establishment of viral latency in the host, rather than a primary ocular infection. Latency develops after the virus enters sensory neurons and travels to sensory ganglia (usually the trigeminal ganglion for ocular disease) by retrograde axoplasmic flow [ 3 ]. The virus remains in ganglia for the lifetime of the host. It has been proposed that HSV-1 latency may also be established in the cornea, although this is controversial [ 4-6 ]. (See "Pathogenesis of herpes simplex virus type 1 infection" .)
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