Evidence map›Paper›PMID 30326825›Full record

ArticleMolecular medicine (Cambridge, Mass.)2018

Hepatitis B virus downregulates vitamin D receptor levels in hepatoma cell lines, thereby preventing vitamin D-dependent inhibition of viral transcription and production.

Neta Gotlieb, Irena Tachlytski, Yelena Lapidot, Maya Sultan, Michal Safran, Ziv Ben-Ari

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  20. COVID-19 Disease and Vitamin D: A Mini-Review.Frontiers in pharmacology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Neta GotliebLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel.
Irena TachlytskiLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel.
Yelena LapidotLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel.
Maya SultanLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel.
Michal SafranLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel.
Ziv Ben-AriLiver Reaserch Laboratory, Sheba Medical Center, Tel Hashomer, 52620, Ramat Gan, Israel. ziv.ben-ari@sheba.health.gov.il.
Sheba Medical Center · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVitamin D is a key immune-modulator that plays a role in the innate and adaptive immune systems. Certain pathogens impair the immune defense by downregulating the vitamin D receptor (VDR) pathway. Low serum levels of vitamin D are associated with increased hepatitis B virus (HBV) replication. Our study aimed to assess the in-vitro relationship between HBV production and Vitamin D signaling pathway and to explore the associated mechanism(s).

methodsHBV transcription and replication was evaluated by qRT-PCR of the HBV-RNA and covalently closed circular DNA (cccDNA). Furthermore, we have transfected the 1.3 X HBV-Luc plasmid to the cells and measured the Luciferase activity using Luminometer. Vitamin D signaling pathway activation was evaluated by measuring the expression levels of VDR, CYP24A1, Tumor necrosis factor α (TNFα) and cathelicidin (CAMP) by qRT-PCR. All assays were performed on HepG2.2.15, HepG2, and HepAD38 cells treated with or without Vitamin D active metabolite: calcitriol.

resultsCalcitriol did not suppress HBV transcription, cccDNA expression or HBV RNA levels in HepG2.2.15 cells. However, VDR transcript levels in HepG2.215 cells were significantly lower compared to HepG2 cells. Similar results were obtained in HepAD38 cell where VDR expression was down-regulated when HBV transcript level was up-regulated. In addition, calcitriol induced VDR-associated signaling, resulting in upregulation of CYP24A1, TNFα and CAMP expression level in HepG2 cells but not in the HepG2.2.15 cells.

conclusionsThese findings indicate that VDR expression is downregulated in HBV-transfected cells, thereby preventing vitamin D from inhibiting transcription and translation of HBV in vitro. HBV might use this mechanism to avoid the immunological defense system by affecting both TNFα and CAMP signaling pathways.

Indexed as

Antimicrobial Cationic PeptidesCalcitriolCarcinoma, HepatocellularCathelicidinsCell Line, TumorDown-RegulationHepatitis B virusHumansLiver NeoplasmsReceptors, CalcitriolRNA, ViralTumor Necrosis Factor-alphaVirus ReplicationAntimicrobial Cationic PeptidesCalcitriolCathelicidinsReceptors, CalcitriolRNA, ViralTumor Necrosis Factor-alphaVDR protein, humanDownregulationHepatitis B virus (HBV)Immune systemVitamin DVitamin D receptor (VDR)

Identifiers

PMID30326825
PMCPMC6192355
OpenAlexW2897955299

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.