MECHANISMS OF STRESS-INDUCED MODULATION OF VIRAL PATHOGENESIS AND IMMUNITY

A murine model of herpes simplex virus (HSV) infection was used to examine the roles of catecholamines and corticosterone in the restraint stress-induced suppression of viral immunity. Treatment of C57BL/6 mice with RU486, a glucocorticoid receptor antagonist, reversed the stress-induced diminution of cellularity in response to local HSV infection. Treatment of mice with both nadolol, a peripherally acting beta-adrenergic antagonist, and RU486 completely reversed the restraint stress-induced suppression of HSV-specific CTL activation. These findings demonstrate that both corticosterone and catecholamine-mediated mechanisms are operative in the stress-induced suppression of anti-viral cellular immunity.