Neural Responses to Injury: Prevention, Protection and Repair; Volume 3: The Neuro-Immunology of Stress, Injury and Infection
Annual rept. 20 Sep 1995-19 Sep 1996
LOUISIANA STATE UNIV NEW ORLEANS
Pagination or Media Count:
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.
- Anatomy and Physiology
- Medicine and Medical Research
- Genetic Engineering and Molecular Biology