Abstract
After recovery from primary herpes simplex virus (HSV) infection of the eye in rabbits, recurrent shedding of virus in the external eye can be produced by the local application of 6-hydroxydopamine (6-HD) and epinephrine. Surgical sympathectomy did not prevent shedding of HSV with 6-HD/epinephrine so the source of the virus in the outer eye induced by adrenergic stimulation is not just the superior cervical ganglia (SCG). Chemical sympathectomy with 6-HD prior to HSV infection of the cornea led to decreased viral replication in the SCG during acute infection but did not interfere with uptake of the virus and latent or low grade infection of the ganglion. Shedding of virus in the outer eye induced by 6-HD/epinephrine was reduced by treatment with the beta-adrenergic blocker, timolol. These experiments strongly suggest that recurrent HSV shedding in the eye induced by catecholamines is due in part to effects on the peripheral (i.e. post synaptic) cells. While the peripheral neurons are the source of virus, it is possible that not all HSV detected in the external eye is due to release of preformed virus from nerve endings.
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