Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes
Cellular and Molecular Life Sciences volume 67, pages4249–4256 (2010) DOI 10.1007/s00018-010-0441-4
Surya Pavan Yenamandra, Ulf Hellman, Bettina Kempkes, Suhas Deoram Darekar, Sabine Petermann, Tom Sculley, George Klein & Elena Kashuba
Epstein-Barr Virus probably causes Long-COVID, CFS, and MS - many studies
VitaminDWiki Items in both categories VIRUS AND VDR
- COVID in hospital stopped by Vitamin D Receptor activators (curcumin, quercetin) – RCT June 2023
- Children with COVID 4X more likely to have poor Vitamin D Receptors (Note: COVID deactivates VDR) – April 2023
- Diabetes 3X more likely if had COVID ICU (VDR was de-activated) - April 2023
- COVID variants protect themselves by deactivating different VDR variants– March 2023
- COVID kids were more likely to have a poor VDR (4.3 X), than low Vitamin D (2.6 X) – Sept 2022
- Cancers are associated with low vitamin D, poor vaccination response and perhaps poor VDR – July 2022
- COVID 3X more likely if a poor Receptor (cells get less Vitamin D from the blood) – July 2022
- Long-COVID is now the biggest COVID concern - many studies
- COVID death 12X more likely if poor Vitamin D Receptor (less D gets to cells) -several studies
- COVID severity, ICU, and mortality all associated with poor vitamin D receptor (but not D, everyone had low D) -Dec 2021
- Different Vitamin D Receptor problems cause different COVID problems - Dec 2021
- COVID-19 severity associated with 3 vitamin D genes – Oct 2021
- Poor Vitamin D receptor blocked Vitamin D from fighting avian influenza viruses (in mice) – July 2021
- Epstein-Barr is yet another virus that deactivates the Vitamin D receptor (COVID later suspected as well)– 2010
- COVID-19 symptoms and comorbidities associated with the type of Vitamin D Receptor – Oct 2021
- Enveloped virus infection (RSV, coronavirus, HIV, etc.) 1.5X more likely if poor Vitamin D Receptor – meta-analysis Dec 2018
- COVID-19 outpatients getting Quercetin nanoemulsion had excellent outcomes (Q increased Vitamin D in cells) – RCT – June 2021
- A virus that most adults have (Cytomegalovirus) decreases the amount of Vitamin D which gets to the cells – Jan 2017
- COVID virus alters the activation of 100 vitamin D related genes in the lung – April 2021
- Common sense COVID-19 risk reduction - masks, social distancing, vitamin D - Oct 2020
- AI is examining 170,000 potential COVID-19 treatments, Vitamin D is one of only 6 found – Sept 4, 2020
- Vitamin D Receptor activation should reduce ARDS associated with COVID-19 - June 2020
- Dengue viral production decreased 1000X if activate Vitamin D Receptor (in lab) – July 2020
- Vitamin D, Quercetin, and Estradiol all increase vitamin D in cells and increase genes which reduce COVID-19 – May 21, 2020
- Quercetin and Vitamin D - Allies Against COVID-19
- Risk of enveloped virus infection is increased 50 percent if poor Vitamin D Receptor - meta-analysis Dec 2018
- Hand, foot, and Mouth disease is 14X more likely if poor Vitamin D Receptor – Oct 2019
- Treating herpes reduced incidence of senile dementia by 10 X (HSV1 reduces VDR by 8X) – 2018
- Severe hand, foot, and mouth virus is 2.9 X more likely if poor Vitamin D receptor – Oct 2018
- Hepatitis B virus reduced by 5X the Vitamin D getting to liver cells in the lab – Oct 2018
- Some enveloped virus are 1.2 X more likely if have a poor Vitamin D Receptor -Aug 2018
- Severe Pertussis is 1.5 times more likely if poor vitamin D receptor – Feb 2016
- Dengue Fever associated with poor vitamin D receptor – July 2002
- Dengue virus 2X to 4X more likely if vitamin D receptor gene problems
2010 study was cited by 54 later studies as of Aug 2022
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Epstein-Barr virus (EBV) is a human gamma herpes virus that infects B cells and induces their transformation into immortalized lymphoblasts that can grow as cell lines (LCLs) in vitro. EBNA-3 is a member of the EBNA-3-protein family that can regulate transcription of cellular and viral genes. The identification of EBNA-3 cellular partners and a study of its influence on cellular pathways are important for understanding the transforming action of the virus. In this work, we have identified the vitamin D receptor (VDR) protein as a binding partner of EBNA-3. We found that EBNA3 blocks the activation of VDR-dependent genes and protects LCLs against vitamin-D3-induced growth arrest and/or apoptosis. The presented data shed some light on the anti-apoptotic EBV program and the role of the EBNA-3-VDR interaction in the viral strategy.