West Nile virus is a pathogen of concern for both human and wildlife health, Although many aspects of the ecology of West Nile virus are well understood, the mechanisms by which this and similar mosquito-borne viruses overwinter and become reinitiated each spring in temperate regions is not known. A thorough understanding of this mechanism is crucial to risk assessment and development of control strategies. One of the hypotheses to explain the mechanism by which this virus persists from year to year is the spring recrudescence of latent virus in avian reservoir hosts. Stress-related immunosuppression is implicated in the recrudescence of latent viruses in birds. We tested the spring recrudescence hypothesis in a controlled laboratory experiment using hatching-year gray catbirds (Dumatella carolinensis) captured in northern Ohio (July–August 2006), Catbirds (n = 60) were experimentally infected (September 2006) and later examined for the effects of immuno-suppression through exogenous hormones and artificially induced migratory disposition, We found no effect of either testosterone or migratory behavior on infection status in any of the treatment birds. Moreover, we detected no viral RNA in the kidney, spleen, brain, or liver upon necropsy at 24 wk postinfection.