The murine model of influenza viral infection was used to evaluate the effects of restraint stress on pathogenesis and survival in the DBA/2 inbred strain of mice. Restraint stress has been associated with an enhanced probability of survival during influenza infection in this strain of mouse. Previous studies suggested that the protective mechanism(s) of stress on mortality might be attributable to elevated levels of circulating glucocorticoids. Subsequent work demonstrated that corticosterone levels alone could not account for the enhanced survival seen in the DBA/2 mice. The present studies examined the role of catecholamines in behavioral stress during influenza infection. It appears that glucocorticoids may play a primary role in trafficking and restriction of inflammation, while catecholamines may play role in limiting activation of virus-specific effector cells. The studies presented here suggest that the interplay between these two physiological response mechanisms needs to be coordinated to optimize development of the immune response to an infection.