Epstein-Barr virus encoded EBNA-3 binds to vitamin D receptor and blocks activation of its target genes.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory study using cell lines with no clinical data.
PubMed 20593215 · doi:10.1007/s00018-010-0441-4
What was done
The authors investigated cellular binding partners of the Epstein-Barr virus (EBV) nuclear protein EBNA-3 and analyzed its effect on cellular pathways in EBV-immortalized lymphoblastoid cell lines (LCLs) in vitro.
What was found
Vitamin D receptor (VDR) was identified as a binding partner of EBNA-3. EBNA-3 blocked activation of VDR-dependent target genes and protected LCLs against vitamin-D3-induced growth arrest and/or apoptosis. The abstract reports no quantitative values or statistical metrics.
Why it matters
The findings demonstrate a direct molecular mechanism by which EBV counteracts vitamin D signaling to promote viral transformation and cell survival.
Limits
The study is restricted to in vitro cell lines and biochemical assays. No in vivo animal models, clinical samples, quantitative effect sizes, or dose-response data are reported in the abstract.
Cited by
- partial Herpes simplex virus and Epstein-Barr virus downregulate or downgrade vitamin D receptors in host cells.