Evidence map›Paper›PMID 27461034›Full record

ArticleScientific reports2016

Stronger enhancer II/core promoter activities of hepatitis B virus isolates of B2 subgenotype than those of C2 subgenotype.

Yanli Qin, Xueshi Zhou, Haodi Jia, Chaoyang Chen, Weifeng Zhao, Jiming Zhang, Shuping Tong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-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

13 citing papers in PubMed, 14 citations in OpenAlex.

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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

7 authors at 5 institutions in 2 countries.

Yanli QinDepartment of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China.
Xueshi ZhouDepartment of Infectious Diseases, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Haodi JiaKey Lab of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Chaoyang ChenKey Lab of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Weifeng ZhaoDepartment of Infectious Diseases, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Jiming ZhangDepartment of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China.
Shuping TongKey Lab of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CNFirst Affiliated Hospital of Soochow University · CNRhode Island Hospital · USSoochow University · CN

Funding

Hepatitis B virus vaccine escape mutantsR01AI116639 · NIAID · RHODE ISLAND HOSPITAL · PI TONG, SHUPING · 2015 to 2019
$1.8M
Hepatitis B virus genotypes B and CR21AI103648 · NIAID · RHODE ISLAND HOSPITAL · PI TONG, SHUPING · 2013 to 2014
$437k
NIAID NIH HHS R01 AI116639NIAID NIH HHS R21 AI103648
6 · The paper itself

Abstract

Hepatitis B virus (HBV) genotype C causes prolonged chronic infection and increased risk for liver cancer than genotype B. Our previous work revealed lower replication capacity of wild-type genotype C2 than B2 isolates. HBV DNA replication is driven by pregenomic RNA, which is controlled by core promoter (CP) and further augmented by enhancer I (ENI) and enhancer II (ENII). DNA fragments covering these regulatory elements were amplified from B2 and C2 isolates to generate luciferase reporter constructs. As ENII is fully embedded in CP, we inserted HBV DNA fragments in the sense orientation to determine their combined activities, and in the antisense orientation to measure enhancer activities alone. Genotype B2 isolates displayed higher ENI+ENII+CP, ENII+CP, and ENII activities, but not ENI or ENI+ENII activity, than C2 isolates. The higher ENII+CP activity was partly attributable to 4 positions displaying genotype-specific variability. Exchanging CP region was sufficient to revert the replication phenotypes of several B2 and C2 clones tested. These results suggest that a weaker ENII and/or CP at least partly accounts for the lower replication capacities of wild-type C2 isolates, which could drive the subsequent acquisition of CP mutations. Such mutations increase genome replication and are implicated in liver cancer development.

Indexed as

Enhancer Elements, GeneticGenotypePromoter Regions, GeneticCell Line, TumorGenetic VariationHepatitis B virusHumansVirus Replication

Identifiers

PMID27461034
PMCPMC4961966
OpenAlexW2479646223

What OpenQuestion holds

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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.