Violeta
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https://journals.aai.org/jimmunol/article/162/8/4998/69399/Glutamate-Augments-Retrovirus-Induced
The mechanisms for activating the hypothalamic-pituitary-adrenal (HPA) axis and the roles glucocorticoids play in the pathogenesis of chronic infectious disease are largely undefined. Using the LP-BM5 model of retrovirus-induced immunodeficiency, we found alterations in HPA axis function, manifested as an increase in circulating levels of adrenocorticotropic hormone and corticosterone, beginning after only 3 mo of infection.
These changes occurred contemporaneously with a shift in the profile of circulating cytokines from a Th1-dominant (IFN-γ) to Th2-dominant (IL-4, IL-10) phenotype.
These findings indicate that HPA axis activation during LP-BM5 retrovirus infection is mediated by the chronic hyperactivation of glutamatergic pathways in the hypothalamus. Through this mechanism, the degree of peripheral immunodeficiency observed in the late-stage disease is profoundly augmented.
I wonder if other viruses do the same thing.
The mechanisms for activating the hypothalamic-pituitary-adrenal (HPA) axis and the roles glucocorticoids play in the pathogenesis of chronic infectious disease are largely undefined. Using the LP-BM5 model of retrovirus-induced immunodeficiency, we found alterations in HPA axis function, manifested as an increase in circulating levels of adrenocorticotropic hormone and corticosterone, beginning after only 3 mo of infection.
These changes occurred contemporaneously with a shift in the profile of circulating cytokines from a Th1-dominant (IFN-γ) to Th2-dominant (IL-4, IL-10) phenotype.
These findings indicate that HPA axis activation during LP-BM5 retrovirus infection is mediated by the chronic hyperactivation of glutamatergic pathways in the hypothalamus. Through this mechanism, the degree of peripheral immunodeficiency observed in the late-stage disease is profoundly augmented.
I wonder if other viruses do the same thing.