Evidence map›Paper›PMID 29242559›Full record

ArticleScientific reports2017

A functional variant in the OAS1 gene is associated with Sjögren's syndrome complicated with HBV infection.

Xianjun Liu, Hongcun Xing, Wenjing Gao, Di Yu, Yuming Zhao, Xiaoju Shi, Kun Zhang, Pingya Li, Jiaao Yu, Wei Xu and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Xianjun LiuThe Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Hongcun XingCollege of Life Sciences, The University of Jilin, Changchun, China.
Wenjing GaoThe Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Di YuThe Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China.
Yuming ZhaoCollege of Life Sciences, The University of Jilin, Changchun, China.
Xiaoju ShiDepartment of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, China.
Kun ZhangThe Research Center, The Second Hospital of Jilin University, Changchun, China.
Pingya LiThe College of Pharmacy, The University of Jilin, Changchun, China.
Jiaao YuDepartment of Burn Surgery, The First Hospital of Jilin University, Changchun, China.
Wei XuDepartment of Clinical Laboratory, The First Hospital of Jilin University, Changchun, China.
Hongli ShanDepartment of Clinical Laboratory, The First Hospital of Jilin University, Changchun, China.
Kaiyu ZhangDepartment of infectious Diseases, The First Hospital of Jilin University, Changchun, China.
Wanguo BaoDepartment of infectious Diseases, The First Hospital of Jilin University, Changchun, China.
Xueqi FuCollege of Life Sciences, The University of Jilin, Changchun, China.
Sirui YangCenter of Pediatrics, Institute of Pediatrics, The First Hospital of Jilin University, Changchun, China. siruiyang@163.com.
Shaofeng WangThe Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, China. shaofengwang@jlu.edu.cn.ORCID 0000-0001-8314-7304
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) has been suspected to contribute to several autoimmune diseases, including Sjögren's syndrome (SS), although the exact mechanism is unknown. The 2'-5' oligoadenylate synthetase (OAS1) is one of the most important components of the immune system and has significant antiviral functions. We studied a polymorphism rs10774671 of OAS1 gene in Han Chinese descent. The minor allele G was significantly associated with a decreased risk for SS, anti-SSA-positive SS, and anti-SSA-positive SS complicated with HBV infection, which have not been seen in anti-SSA-negative SS and HBcAb-negative SS patients. Gene expression analysis showed that the risk-conferring A allele was correlated with lower expression of p46 and increased expression of p42, p48, and p44. A functional study of enzymatic activities revealed that the p42, p44, and p48 isoforms display a reduced capacity to inhibit HBV replication in HepG2 cells compared to the normal p46 isoform. Our data demonstrated that the functional variant, rs10774671, is associated with HBV infection and anti-SSA antibody-positive SS. The SAS variant switches the primary p46 isoform to three alternatives with decreased capacities to inhibit HBV replication. These data indicated that individuals harboring the risk allele might be susceptible to hepatitis B infection and SS development.

Indexed as

Polymorphism, Single Nucleotide2',5'-Oligoadenylate SynthetaseAdultAllelesCase-Control StudiesFemaleGene Expression RegulationGenetic Predisposition to DiseaseHepatitis BHumansMaleSjogren's Syndrome2',5'-Oligoadenylate SynthetaseOAS1 protein, human

Identifiers

PMID29242559
PMCPMC5730593
OpenAlexW2771966708

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Registered trials

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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.