STRESS-INDUCED REACTIVATION OF LATENT HERPES-SIMPLEX VIRUS-INFECTION IN RAT LUMBAR DORSAL-ROOT GANGLIA

Clinical reports suggest that stress precipitates recurrent cutaneous Herpes simplex virus (HSV) infection, presumably by reactivating laten t infection in sensory ganglia with subsequent centrifugal axonal spre ad to the skin. As an initial test of this hypothesis, rats with laten t HSV, type-1, (HSV-1) infection in lumbar dorsal root ganglia (DRG) w ere exposed to a well-characterized acute stressor that produced gastr ic ulcers (U) and elevated plasma corticosterone (CS) concentrations. Stress-induced reactivation of latent HSV infection was suggested by t he earlier appearance of cytopathic effect (CPE) in human foreskin fib roblast monolayers co-cultivated with ganglia from stressed rats than from nonstressed ones (4.5 +/- 0.2 and 6.4 +/- 0.4 [mean +/- SEM] days respectively; p < 0.001). No CPE was detected in monolayers co-cultiv ated with ganglia from non-infected rats. These initial results sugges t that acute stress reactivates latent HSV-1 ganglionic infection.