Autonomic and glucocorticoid associations with the steady-state expression of latent Epstein-Barr virus
Identifieur interne : 000278 ( PascalFrancis/Corpus ); précédent : 000277; suivant : 000279Autonomic and glucocorticoid associations with the steady-state expression of latent Epstein-Barr virus
Auteurs : John T. Cacioppo ; Janice K. Kiecolt-Glaser ; William B. Malarkey ; Bryon F. Laskowski ; Leigh Ann Rozlog ; Kirsten M. Poehlmann ; Mary H. Burleson ; Ronald GlaserSource :
- Hormones and behavior [ 0018-506X ] ; 2002.
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- Pascal (Inist)
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- KwdEn :
Abstract
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 culture, 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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Format Inist (serveur)
NO : | PASCAL 02-0546905 INIST |
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ET : | Autonomic and glucocorticoid associations with the steady-state expression of latent Epstein-Barr virus |
AU : | CACIOPPO (John T.); KIECOLT-GLASER (Janice K.); MALARKEY (William B.); LASKOWSKI (Bryon F.); ROZLOG (Leigh Ann); POEHLMANN (Kirsten M.); BURLESON (Mary H.); GLASER (Ronald) |
AF : | University of Chicago/Chicago, Illinois/Etats-Unis (1 aut.); Ohio State University College of Medicine/Ohio/Etats-Unis (2 aut., 3 aut., 4 aut., 5 aut., 8 aut.); University of Houston/Houston, Texas/Etats-Unis (6 aut.); Arizona State University/Tempe, Arizona/Etats-Unis (7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Hormones and behavior; ISSN 0018-506X; Coden HOBEAO; Etats-Unis; Da. 2002; Vol. 42; No. 1; Pp. 32-41; Bibl. 1 p.1/4 |
LA : | Anglais |
EA : | 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 culture, 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. |
CC : | 002A26C08; 002A26C03; 002A26G08 |
FD : | Femelle; Virus Epstein Barr; Immunité cellulaire; ACTH; Hydrocortisone; Noradrénaline; Stress; Système nerveux autonome; Homme; Adrénaline; Réponse immune |
FG : | Gammaherpesvirinae; Herpesviridae; Virus; Hormone adénohypophysaire; Glucocorticoïde; Hormone surrénalienne; Catécholamine |
ED : | Female; Epstein Barr virus; Cellular immunity; Adrenocorticotropic hormone; Hydrocortisone; Norepinephrine; Stress; Autonomic nervous system; Human; Epinephrine; Immune response |
EG : | Gammaherpesvirinae; Herpesviridae; Virus; Adenohypophyseal hormone; Glucocorticoid; Adrenal hormone; Catecholamine |
SD : | Hembra; Epstein Barr virus; Inmunidad celular; ACTH; Hidrocortisona; Noradrenalina; Estrés; Sistema nervioso autónomo; Hombre; Adrenalina; Respuesta inmune |
LO : | INIST-14364.354000109242160040 |
ID : | 02-0546905 |
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Pascal:02-0546905Le document en format XML
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<front><div type="abstract" xml:lang="en">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 culture, 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.</div>
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<s5>05</s5>
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<fC03 i1="05" i2="X" l="SPA"><s0>Hidrocortisona</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Noradrénaline</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Norepinephrine</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Noradrenalina</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Stress</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Stress</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Estrés</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Système nerveux autonome</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Autonomic nervous system</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Sistema nervioso autónomo</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
<s5>54</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Human</s0>
<s5>54</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0>
<s5>54</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Adrénaline</s0>
<s2>NK</s2>
<s5>57</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Epinephrine</s0>
<s2>NK</s2>
<s5>57</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Adrenalina</s0>
<s2>NK</s2>
<s5>57</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Réponse immune</s0>
<s5>60</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Immune response</s0>
<s5>60</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Respuesta inmune</s0>
<s5>60</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Gammaherpesvirinae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Gammaherpesvirinae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Gammaherpesvirinae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Herpesviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Herpesviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Herpesviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Hormone adénohypophysaire</s0>
<s5>29</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Adenohypophyseal hormone</s0>
<s5>29</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Hormona adenohipofisaria</s0>
<s5>29</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Glucocorticoïde</s0>
<s5>32</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Glucocorticoid</s0>
<s5>32</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Glucocorticoide</s0>
<s5>32</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Hormone surrénalienne</s0>
<s5>33</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Adrenal hormone</s0>
<s5>33</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Hormona suprarrenal</s0>
<s5>33</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>35</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>35</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>35</s5>
</fC07>
<fN21><s1>322</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 02-0546905 INIST</NO>
<ET>Autonomic and glucocorticoid associations with the steady-state expression of latent Epstein-Barr virus</ET>
<AU>CACIOPPO (John T.); KIECOLT-GLASER (Janice K.); MALARKEY (William B.); LASKOWSKI (Bryon F.); ROZLOG (Leigh Ann); POEHLMANN (Kirsten M.); BURLESON (Mary H.); GLASER (Ronald)</AU>
<AF>University of Chicago/Chicago, Illinois/Etats-Unis (1 aut.); Ohio State University College of Medicine/Ohio/Etats-Unis (2 aut., 3 aut., 4 aut., 5 aut., 8 aut.); University of Houston/Houston, Texas/Etats-Unis (6 aut.); Arizona State University/Tempe, Arizona/Etats-Unis (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Hormones and behavior; ISSN 0018-506X; Coden HOBEAO; Etats-Unis; Da. 2002; Vol. 42; No. 1; Pp. 32-41; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>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 culture, 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.</EA>
<CC>002A26C08; 002A26C03; 002A26G08</CC>
<FD>Femelle; Virus Epstein Barr; Immunité cellulaire; ACTH; Hydrocortisone; Noradrénaline; Stress; Système nerveux autonome; Homme; Adrénaline; Réponse immune</FD>
<FG>Gammaherpesvirinae; Herpesviridae; Virus; Hormone adénohypophysaire; Glucocorticoïde; Hormone surrénalienne; Catécholamine</FG>
<ED>Female; Epstein Barr virus; Cellular immunity; Adrenocorticotropic hormone; Hydrocortisone; Norepinephrine; Stress; Autonomic nervous system; Human; Epinephrine; Immune response</ED>
<EG>Gammaherpesvirinae; Herpesviridae; Virus; Adenohypophyseal hormone; Glucocorticoid; Adrenal hormone; Catecholamine</EG>
<SD>Hembra; Epstein Barr virus; Inmunidad celular; ACTH; Hidrocortisona; Noradrenalina; Estrés; Sistema nervioso autónomo; Hombre; Adrenalina; Respuesta inmune</SD>
<LO>INIST-14364.354000109242160040</LO>
<ID>02-0546905</ID>
</server>
</inist>
</record>
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