AI Article Synopsis
- Inflammatory mediators like TNFalpha can trigger active human cytomegalovirus (HCMV) infection, but recent findings show that stress, like that from acute myocardial infarction, can also activate HCMV in latently infected individuals.
- The study demonstrates that catecholamines (e.g., epinephrine) stimulate the HCMV immediate-early enhancer through beta-2 adrenergic receptors, activating a specific signaling pathway (cAMP/PK-A) that increases the binding of key transcription factors.
- Overall, HCMV can be reactivated under stress conditions, suggesting similar behavior to other herpes viruses like HSV-1 and VZV.
Article Abstract
Recently, inflammatory mediators such as TNFalpha 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 beta-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.
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| http://dx.doi.org/10.1006/viro.2000.0367 | DOI Listing |
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