Author: Nicolas Bazan

Publisher:

Published: 1997

Total Pages: 252

ISBN-13:

The hypothesis on which this investigation is based is that stressors such' as transient temperature changes and restraint signal the central nervous system eliciting the release of catecholamines and adrenal steroids which, in turn, affect the immune system resulting in the reactivation of latent viruses. Employing a mouse model of stress-induced reactivation of herpes simplex virus type 1 (HSV-1), we are determining the time course of viral reactivation relative to the alteration of immune parameters including lymphocyte functions and numbers. Specifically, we are correlating the expression of various immunomodulatory cytokine genes with the levels of neuroendocrine monoamines, as well as the activation of the hypothalamic- pituitary-adrenal (HPA) axis and relating these to the reactivation of infectious virus in the nervous system. Alterations in serum corticosterone and shifts in monoamines in the brains, trigeminal ganglia, and brain stems of latently infected and reactivated mice following the application of stress are being studied. Differences between control (not stressed) and stressed animals are being determined relative to the incidence of viral reactivation and the affect of stress on immunological regulation of the reactivation process. The knowledge gained from this investigation will provide an understanding of the interaction between the nervous system, the neuroendocrine system, and the immune system during times of stress at the molecular and cellular levels.