A Novel Link between Stress and Human Cytomegalovirus (HCMV) Infection: Sympathetic Hyperactivity Stimulates HCMV Activation

Recently, inflammatory mediators such as TNFα were identified as triggering active human cytomegalovirus (HCMV) infection. Here, we demonstrate that a highly stressful event in the absence of systemic inflammation, as observed in patients with acute myocardial infarction, leads to the development of...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2000-07, Vol.272 (2), p.357-365
Main Authors: Prösch, Susanna, Wendt, Cornelia E.C., Reinke, Petra, Priemer, Christina, Oppert, Michael, Krüger, Detlev H., Volk, Hans-Dieter, Döcke, Wolf-Dietrich
Format: Article
Language:English
Subjects:
Activating Transcription Factor 1
Adult
Aged
Catecholamines - metabolism
Cell Line
Cyclic AMP Response Element-Binding Protein - metabolism
Cyclic AMP-Dependent Protein Kinases - metabolism
Cytomegalovirus - enzymology
Cytomegalovirus - physiology
Cytomegalovirus Infections - metabolism
Cytomegalovirus Infections - virology
DNA-Binding Proteins
Enhancer Elements, Genetic - genetics
Epinephrine - pharmacology
Female
Gene Expression Regulation, Viral - drug effects
Human cytomegalovirus
Humans
Male
Middle Aged
Monocytes - metabolism
Myocardial Infarction - metabolism
Myocardial Infarction - virology
Promoter Regions, Genetic - genetics
Receptors, Adrenergic, beta-2 - physiology
Stress, Physiological - enzymology
Stress, Physiological - virology
Sympathetic Nervous System - virology
Transcription Factors - biosynthesis
Transcription Factors - metabolism
Virus Activation
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Summary:Recently, inflammatory mediators such as TNFα were identified as triggering active human cytomegalovirus (HCMV) infection. Here, we demonstrate that a highly stressful event in the absence of systemic inflammation, as observed in patients with acute myocardial infarction, leads to the development of an active HCMV infection in latently infected patients. Elucidating the molecular mechanism of virus activation, we could show that catecholamines directly stimulate the HCMV immediate-early (IE) enhancer/promoter in monocytic cells via β-2 adrenergic receptors. Subsequent activation of the cAMP/PK-A-signaling pathway results in enhanced synthesis and binding of the transcription factor CREB-1/ATF-1 to the cAMP-responsive elements within the IE enhancer. Epinephrine also enhanced HCMV gene expression in infected THP-1 cells by about 50% in three of four experiments. These data suggest that HCMV, like HSV-1 and VZV, can be (re)activated under stress conditions.
ISSN:0042-6822
1096-0341
DOI:10.1006/viro.2000.0367