TY - JOUR
T1 - Autonomic and glucocorticoid associations with the steady-state expression of latent Epstein-Barr virus
AU - Cacioppo, John T.
AU - Kiecolt-Glaser, Janice K.
AU - Malarkey, William B.
AU - Laskowski, Bryon F.
AU - Rozlog, Leigh Ann
AU - Poehlmann, Kirsten M.
AU - Burleson, Mary
AU - Glaser, Ronald
N1 - Funding Information:
We thank the nursing staff of the Clinical Research Center for the blood draws and Sue Moseley, Julianne Dorne, Karen Brown, Hsiao-yin Mao, and Marco Vasquez for their expert technical assistance. This research was partially supported by Grants AG11585 from the National Institute of Aging, MH18831, MH44660, MH42096, and MHS0538 from the National Institute of Mental Health, a supplement to MH42096 from the Office of Women’s Health, General Clinical Research Center Grant M01RR0034, the Ohio State University Comprehensive Cancer Center core grant from the NCI, CA16058, and the Mind–Body Research Network of the John D. and Catherine T. MacArthur Foundation.
PY - 2002/8
Y1 - 2002/8
N2 - Previous studies have demonstrated the impact of psychological stress on the steady-state expression/reactivation of latent Epstein-Barr virus (EBV). Stress-induced decrements in the cellular immune response result in less control over the expression of the latent virus, resulting in increases in antibody to the virus. In Study 1, we investigated whether the steady-state expression of latent EBV in vivo differed between high and low stress reactors, as defined by sympathetic cardiac reactivity. Autonomic activity and antibody titers to Epstein-Barr virus capsid antigen (VCA) were measured in 50 elderly women latently infected with EBV. Results revealed that women who were high stress reactors were characterized by higher antibody titers to the latent virus than low stress reactors. High reactors tended to show larger stress-related increases in cortisol than low reactors, but the differences were not significant. Daily stressors can activate the autonomic nervous system and promote the release of pituitary and adrenal hormones, especially in high reactors. Glucocorticoid hormones have been shown to reactivate EBV in vitro from cells latently infected with the virus. We hypothesized that absolute levels of plasma cortisol may not be the only explanation for stress-induced reactivation of latent EBV and that the diurnal changes in the production of cortisol may be an important factor in these interactions. To examine the feasibility of this hypothesis, an in vitro study was conducted (Study 2) to determine whether changing glucocorticoid concentrations in the medium, in which EBV latently infected cells were cultured, to mimic diurnal changes in plasma cortisol concentrations would enhance the reactivation of the latent virus. Cells latently infected with EBV were exposed to either constant or varying concentrations of the synthetic glucocorticoid hormone dexamethasone (Dex), for 72 h. Results revealed a three- to eightfold enhancement of reactivation of latent EBV in cells pulsed with varying Dex concentrations when compared with cells exposed to a constant and/or a higher mean level of one Dex concentration. Together, these studies raise the possibility that differences in the kinetics of glucocorticoid concentrations may contribute to differences in the reactivation of latent EBV.
AB - Previous studies have demonstrated the impact of psychological stress on the steady-state expression/reactivation of latent Epstein-Barr virus (EBV). Stress-induced decrements in the cellular immune response result in less control over the expression of the latent virus, resulting in increases in antibody to the virus. In Study 1, we investigated whether the steady-state expression of latent EBV in vivo differed between high and low stress reactors, as defined by sympathetic cardiac reactivity. Autonomic activity and antibody titers to Epstein-Barr virus capsid antigen (VCA) were measured in 50 elderly women latently infected with EBV. Results revealed that women who were high stress reactors were characterized by higher antibody titers to the latent virus than low stress reactors. High reactors tended to show larger stress-related increases in cortisol than low reactors, but the differences were not significant. Daily stressors can activate the autonomic nervous system and promote the release of pituitary and adrenal hormones, especially in high reactors. Glucocorticoid hormones have been shown to reactivate EBV in vitro from cells latently infected with the virus. We hypothesized that absolute levels of plasma cortisol may not be the only explanation for stress-induced reactivation of latent EBV and that the diurnal changes in the production of cortisol may be an important factor in these interactions. To examine the feasibility of this hypothesis, an in vitro study was conducted (Study 2) to determine whether changing glucocorticoid concentrations in the medium, in which EBV latently infected cells were cultured, to mimic diurnal changes in plasma cortisol concentrations would enhance the reactivation of the latent virus. Cells latently infected with EBV were exposed to either constant or varying concentrations of the synthetic glucocorticoid hormone dexamethasone (Dex), for 72 h. Results revealed a three- to eightfold enhancement of reactivation of latent EBV in cells pulsed with varying Dex concentrations when compared with cells exposed to a constant and/or a higher mean level of one Dex concentration. Together, these studies raise the possibility that differences in the kinetics of glucocorticoid concentrations may contribute to differences in the reactivation of latent EBV.
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U2 - 10.1006/hbeh.2002.1801
DO - 10.1006/hbeh.2002.1801
M3 - Article
C2 - 12191645
AN - SCOPUS:0036672705
SN - 0018-506X
VL - 42
SP - 32
EP - 41
JO - Hormones and Behavior
JF - Hormones and Behavior
IS - 1
ER -