Human cytomegalovirus infection downregulates vitamin-D receptor in mammalian cells
The Journal of Steroid Biochemistry and Molecular Biology, Vol 165, Part B, Jan 2017, Pages 356–362, http://dx.doi.org/10.1016/j.jsbmb.2016.08.002
Franz J.J. Riedera, Charlotte Gröschelb, Marie-Theres Kastnera, Karin Kosulinc, Johannes Laengled, Rene Zadnikare, Rodrig Marculescue, Martina Schneidera, Thomas Lionc, f, Michael Bergmannd, Enikö Kallayb, Christoph Steiningera,
Highlights
•Vitamin D is essential for the human body including antimicrobial responses.
•Cytomegalovirus infection downregulates VDR expression in vitro..
•Expression of CYP24A1 decreases and of CYP27B1 increases in parallel.
•VDR expression is not downregulated during influenza virus or adenovirus replication.
•Cytomegalovirus may also influence VDR expression in vivo.
Vitamin D (VD) is essential for the human body and involved in a wide variety of critical physiological processes including bone, muscle, and cardiovascular health, as well as innate immunity and antimicrobial responses. Here, we elucidated the significance of the VD system in cytomegalovirus (CMV) infection, which is one of the most common opportunistic infections in immunocompromised or -suppressed patients. We found that expression of vitamin D receptor (VDR) was downregulated in CMV-infected cells within 12 h [hrs] post infection [p.i.] to 12% relative to VDR expression in mock-infected fibroblasts and did not recover during the CMV replication cycle of 96 h. None of the biologically active metabolites of VD, cholecalciferol, calcidiol, or calcitriol, inhibit CMV replication significantly in human fibroblasts. In a feedback loop, expression of CYP24A1 dropped to 3% by 12 h p.i. and expression of CYP27B1 increased gradually during the replication cycle of CMV to 970% probably as a consequence of VDR inhibition.
VDR expression was not downregulated during influenza virus or adenovirus replication.
The potent synthetic vitamin D analog EB-1089 was not able to inhibit CMV replication or antagonize its effect on VDR expression. Only CMV replication, and none of the other viral pathogens evaluated, inhibited the vitamin D system in vitro. In view of the pleiotropism of VDR, CMV-mediated downregulation may have far-reaching virological, immunological, and clinical implications and thus warrant further evaluations in vitro and in vivo.
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Appears that many people have herpes and do not know it.
Herpes does not appear to lower the blood levels of vitamin D
Herpes appears to greatly restricts vitamin D getting to cells by downregulating the VDR
See also Vitamin D Life
See also web
- https://en.wikipedia.org/wiki/Epidemiology_of_herpes_simplex WikiPedia 2016
"About 1 in 5 Americans (16.2%) aged 14 to 49 is infected with HSV-2. HSV-2 prevalence was nearly twice as high among women (20.9%) than men (11.5%), and was more than three times higher among blacks (39.2%) than non-Hispanic whites (12.3%). The most affected group was black women, with a prevalence rate of 48%."
"Although many people infected with HSV develop labial or genital lesions (herpes simplex), the majority are either undiagnosed or display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes." - Herpes Zoster Rates Are Increasing, but Why? Medscape 2014
" In the United States, herpes zoster rates have increased by 39% from 1992 to 2010 among adults older than 65 years of age"