Physiological Relationships Among Stress, Viruses, and Cancer in Experimental Animals

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Abstract
Anxiety-induced psychoneural stimulation, via the hypothalamic-pituitary axis, activates the adrenal cortex to release corticosteroids, which elicit various alterations of corticoid-sensitive cell-mediated immunologic processes. Stress sensitive murine tumor-host experimental models have been utilized to demonstrate various effects of stress upon aspects of tumor development. Although many of the observed anxiety-induced alterations of tumor-related parameters can be interpreted in terms of corticoid-induced modifications of immune functions, other observations are more difficult to interpret, and may be caused in part by corticosteroid-independent modulation of lymphocyte functions. In the case of tumors induced by oncogenic viruses, anxiety-induced plasma corticoid elevations may also act independently of the immune system to stimulate tumor development via hormone binding sites on proviral DNA. Rigorously controlled environmental and experimental conditions are fundamental for the demonstration and interpretation of stress-related phenomena. Technical prerequisites include protective animal facilities, special handling procedures, the use of nontraumatic stressors, and the recognition of vital psychosocial, coping and timing factors. Various biologic factors, such as sex, genetic substrain differences and common interfering viral infections, must also be controlled or taken into consideration.