Evidence map›Paper›PMID 25690916›Full record

ArticleJournal of medical virology2015

Endogenous antiviral microRNAs determine permissiveness for hepatitis B virus replication in cultured human fetal and adult hepatocytes.

Mukesh Kumar, Yogeshwar Sharma, Sriram Bandi, Sanjeev Gupta

Open access · greenAbstract read
In one paragraph

Article in Journal of medical virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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

4 authors at 1 institution in 1 country.

Mukesh KumarMarion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York.
Yogeshwar Sharma
Sriram Bandi
Sanjeev Gupta
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Special Animal CoreP30DK041296 · NIDDK · YESHIVA UNIVERSITY · PI WOLKOFF, ALLAN W · 1989 to 2018
$22.9M
Transplantation of Endothelial CellsR01DK071111 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GUPTA, SANJEEV · 2006 to 2016
$3.6M
Cell transplantation and inflammationR01DK088561 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GUPTA, SANJEEV · 2011 to 2014
$1.7M
NCI NIH HHS P30 CA013330NIDDK NIH HHS P30 DK041296NIDDK NIH HHS P30 DK-41296NIDDK NIH HHS R01 DK-071111NIDDK NIH HHS R01 DK071111NIDDK NIH HHS R01 DK088561NIDDK NIH HHS R01 DK-088581
6 · The paper itself

Abstract

Superior cell culture models for hepatitis B virus (HBV) will help advance insights into host-virus interactions. To identify mechanisms regulating HBV replication, this study used cultured human HepG2 cells and adult or fetal hepatocytes transduced with adenoviral vector to express HBV upstream of green fluorescent protein. The vector efficiently transduced all cell types. In HepG2 cells, replicative viral intermediates, nucleocapsid-associated HBcAg, and HBsAg were expressed. However, in fetal or adult hepatocytes, pregenomic HBV RNA and viral RNAs were expressed, but nucleocapsid-associated HBcAg in cells or HBsAg in culture medium were absent, indicating interruptions in viral replication due to possible microRNA-related interference. MicroRNA profiling demonstrated that a large number of microRNAs with antiviral potential were differentially expressed in hepatocytes after culture. In transfection assays using HepG2 cells, candidate antiviral microRNAs, e.g., hsa-miR-24 or hsa-miR-638 decreased the levels of HBV transcripts or HBV gene products. Since candidate microRNAs could have targeted interferon response genes as an alternative explanation interferon signaling was examined. However, HBV replication in cultured hepatocytes was not restored despite successful inhibition of JAK1/2-STAT signaling by the inhibitor, ruxolitinib. Therefore, HBV was unable to complete replication in cultured hepatocytes due to expression of multiple antiviral microRNAs. This mechanism should help understand restrictions in HBV replication for developing HBV models in cultured cells while providing frameworks for pathophysiological studies of HBV replication in subsets of hepatocytes or stem/progenitor cells during hepatitis.

Indexed as

Cell LineCells, CulturedCluster AnalysisGene ExpressionGene Expression ProfilingHepatitis B virusHepatocytesHep G2 CellsHumansInterferonsMicroRNAsRNA InterferenceRNA, MessengerRNA, ViralSignal TransductionTransfectionInterferonsMicroRNAsRNA, MessengerRNA, Viralgene expressionhepatitisinteractionliver

Identifiers

PMID25690916
PMCPMC4536901
OpenAlexW1711873436

What OpenQuestion holds

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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.