Pathogen burden and cortisol profiles over the day

Steptoe, Andrew; Gylfe, Åsa; Shamaei-Tousi, Alireza; Bergström, Sven; Henderson, Brian E.

doi:10.1017/s0950268809002738

Cited by 7 publications

(5 citation statements)

References 70 publications

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“…Significantly, research has shown that CMV can directly increase cortisol production by its ability to infect and replicate in human adrenocortical cells, where it causes steroidogenesis (Trevisan et al, 2009). In conjunction, this group has previously reported an aberrant cortisol release in healthy CMV-positive individuals involving a flattened circadian decline (Steptoe et al, 2009), which implies a more constant level of exposure to the hormone. Such a flattened secretion pattern has repeatedly been associated with impaired immunity and enhanced inflammatory activity, both in healthy and clinical populations (Edwards et al, 2010; Matthews et al, 2006; Miller et al, 2008), which, in turn, may further promote elevated viral reactivation.…”

Section: Discussionmentioning

confidence: 91%

Cytomegalovirus is associated with reduced telomerase activity in the Whitehall II cohort

Dowd

Bosch

Steptoe

et al. 2013

Experimental Gerontology

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Telomere length and telomerase activity have received increased attention as markers of cellular aging, but the determinants of inter-individual variation in these markers are incompletely understood. Cytomegalovirus (CMV) infection may be particularly important for telomere and telomerase dynamics due to its dramatic impact on peripheral blood lymphocyte composition, i.e., increasing the number and proportions of highly differentiated T cells that are characterized by shorter telomere length (TL) and lowered telomerase activity (TA). However, the possible relationship between CMV infection and leukocyte TL and TA has not been well-examined in vivo. This study examined the associations of CMV seropositivity and CMV IgG antibodies with leukocyte (TL) and (TA) in a sample of 434 healthy individuals (ages 53–76) from the Whitehall II cohort. Positive CMV serostatus was significantly associated with lower TA among women, and higher CMV IgG antibody levels were associated with lower TA in the overall sample. However, neither CMV seropositivity nor CMV IgG antibody levels (reflecting subclinical reactivation) among the seropositive were significantly associated with TL. These associations were robust to adjustment for age, employment grade, BMI, and smoking status. The results demonstrate that CMV seropositivity and subclinical reactivation predict lower TA. Future longitudinal studies should test whether the association of CMV with lower TA contributes to accelerated telomere shortening over time.

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Section: Discussionmentioning

confidence: 91%

Cytomegalovirus is associated with reduced telomerase activity in the Whitehall II cohort

Dowd

Bosch

Steptoe

et al. 2013

Experimental Gerontology

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“…Indeed, in vivo reactivation of different herpesviruses may involve multiple neuroendocirine interactions (Glaser et al, 1985; Kiecolt-Glaser et al, 1984; Kiecolt-Glaser and Glaser, 1987; Yang et al, 2010). Further work is necessary to understand these complex processes (Matalka et al, 2000; Mehta and Pierson, 2007; Steptoe et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Fatigue and herpesvirus latency in women newly diagnosed with breast cancer

Fagundes¹,

Glaser²,

Alfano³

et al. 2012

Brain, Behavior, and Immunity

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Fatigue is a notable clinical problem in cancer survivors, and understanding its pathophysiology is important. The current study sought to determine biomarkers of fatigue that exist before cancer treatment. Relationships between the expression of latent Epstein–Barr virus (EBV) and cytomegalovirus (CMV) and fatigue were examined in 158 women newly diagnosed with breast cancer or awaiting a positive diagnostic result. Higher CMV antibody titers, but not EBV antibody titers, were associated with a greater likelihood of being fatigued. Associations between fatigue and higher CMV antibody titers remained after controlling for alcohol use, smoking, comorbidities, depressive symptoms, age, BMI, cancer stage, and sleep problems. More sleep problems and higher levels of depressive symptoms were also associated with a greater likelihood of being fatigued. CMV antibody titers, but not EBV antibody titers, were associated with higher levels of C-reactive protein (CRP), but CRP was not associated with fatigue. When the cellular immune system is compromised, reactivation of latent herpesviruses may fuel chronic inflammatory responses. Prior work has suggested that fatigue may be related to inflammation and its associated sickness behaviors; accordingly, our findings may be tapping into this same physiological substrate.

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“…Neuroendocine mechanisms could also play a role in this association. Using a summary index of positive serologies against three common infections (CMV, C. pneumoniae , and HSV 1) among 317 healthy volunteers, there was a flattening of the normal slope of decline in salivary cortisol levels among those with a higher pathogen burden, independently of other demographic and socioeconomic variables 60. A decrease in cortisol decline over the course of the day has been associated with coronary artery disease 61.…”

Section: Mechanismsmentioning

confidence: 99%

Infectious Burden: A New Risk Factor and Treatment Target for Atherosclerosis

Elkind¹

2010

IDDT

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Atherosclerosis is a chronic inflammatory process, and several common bacterial and viral infections have been hypothesized to contribute to the inflammation of the vascular wall that leads to atherosclerosis. More recently, investigators have found preliminary evidence that the aggregate burden of these chronic infections, rather than any single organism, may contribute to atherosclerosis and risk of clinical vascular events, including ischemic stroke. This aggregate burden of infections, which has been variably labeled "infectious burden" or "pathogen burden," may be associated with stroke through mechanisms independent of atherosclerosis, as well, including platelet aggregation and endothelial dysfunction. Host factors, moreover, may interact with infectious burden to modify the risk of disease associated with these infections. Currently there is no commonly accepted group of organisms or method of assessing infectious burden, and not all studies confirm an association of infection and stroke risk. Nonetheless, if infectious burden does play a role in atherosclerosis or stroke, it is plausible that preventive anti-infective treatment, such as vaccination, or antibiotics, would reduce the risk of incident or recurrent stroke. While influenza vaccination has been recommended to prevent recurrence among those with coronary disease, similar recommendations for stroke patients have not yet been made. Large scale randomized clinical trials of macrolide antibiotics for coronary patients, moreover, have been negative. Further studies are needed, however, to determine whether an association between infectious burden and stroke exists, and whether infectious burden may be a target for intervention.

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Pathogen burden and cortisol profiles over the day

Cited by 7 publications

References 70 publications

Cytomegalovirus is associated with reduced telomerase activity in the Whitehall II cohort

Cytomegalovirus is associated with reduced telomerase activity in the Whitehall II cohort

Fatigue and herpesvirus latency in women newly diagnosed with breast cancer

Infectious Burden: A New Risk Factor and Treatment Target for Atherosclerosis

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