Twelve nulliparous, sexually mature heifers free of antibodies to infectious bovine rhinotracheitis (IBR) virus were exposed intranasally to Colorado strain IBR virus. After 3 mos, when the postexposure antibody titers had stabilized, the heifers were divided into three groups. Individuals in each group were treated with either saline, dexamethasone or follicle stimulating hormone (FSH) for five consecutive days. Blood samples were taken at predetermined intervals for isolation of virus, and for determination of serum cortisol levels. No changes occurred in the saline-treated group, except that one heifer had a slightly elevated serum neutralizing antibody titer. Recrudescense of typical clinical lesions was observed in the dexamethasone-treated group, and the IBR virus was isolated from nasal swab samples taken from all heifers. In the FSH-treated group, no changes occurred, with the exception of slightly reduced serum cortisol levels. Results indicate that FSH-induced superovulation does not cause reactivation of IBR virus in heifers previously infected by the intranasal route, and has no effect on serum neutralizing anti-IBR virus antibody titers.