Evidence map›Paper›PMID 26585041›Full record

ArticleScientific reports2015

Hepatitis B virus spliced variants are associated with an impaired response to interferon therapy.

Jieliang Chen, Min Wu, Fan Wang, Wen Zhang, Wei Wang, Xiaonan Zhang, Jiming Zhang, Yinghui Liu, Yi Liu, Yanling Feng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

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  11. TheJournal of virology · 2024
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  18. [Expert consensus on measurement and clinical application of serum HBV RNA in patients with chronic HBV infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Article
  19. Article
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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

13 authors at 4 institutions in 1 country.

Jieliang ChenKey Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, China.
Min WuShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Fan WangShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Wen ZhangKey Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, China.
Wei WangShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Xiaonan ZhangShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Jiming ZhangHuashan Hospital affiliated to Fudan University, China.
Yinghui LiuKey Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, China.
Yi LiuShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Yanling FengShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Ye ZhengShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Yunwen HuShanghai Public Health Clinical Center, Shanghai Medical College of Fudan University, China.
Zhenghong YuanKey Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Shanghai Medical College of Fudan University, China.
Shanghai Medical College of Fudan University · CNShanghai Public Health Clinical Center · CNFudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During hepatitis B virus (HBV) replication, spliced HBV genomes and splice-generated proteins have been widely described, however, their biological and clinical significance remains to be defined. Here, an elevation of the proportion of HBV spliced variants in the sera of patients with chronic hepatitis B (CHB) is shown to correlate with an impaired respond to interferon-α (IFN-α) therapy. Transfection of the constructs encoding the three most dominant species of spliced variants into cells or ectopic expression of the two major spliced protein including HBSP and N-terminal-truncated viral polymerase protein result in strong suppression of IFN-α signaling transduction, while mutation of the major splicing-related sites of HBV attenuates the viral anti-IFN activities in both cell and mouse models. These results have associated the productions of HBV spliced variants with the failure response to IFN therapy and illuminate a novel mechanism where spliced viral products are employed to resist IFN-mediated host defense.

Indexed as

RNA SplicingAdolescentAdultAnimalsAntiviral AgentsBase SequenceCell Line, TumorDNA, ViralDrug Resistance, ViralFemaleHepatitis B, ChronicHepatitis B virusHep G2 CellsHost-Pathogen InteractionsHumansInterferon-alphaAntiviral AgentsDNA, ViralInterferon-alphaViral Proteins

Identifiers

PMID26585041
PMCPMC4653653
OpenAlexW2177010973

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.