Evidence map›Paper›PMID 25945020›Full record

ArticleWorld journal of gastroenterology2015

Hepatitis B virus preS1 deletion is related to viral replication increase and disease progression.

Seoung-Ae Lee, Ki-Jeong Kim, Hong Kim, Won-Hyuk Choi, Yu-Sub Won, Bum-Joon Kim

Abstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2015. 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
–field-weighted citation impact
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.

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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.

Seoung-Ae LeeSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.
Ki-Jeong KimSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.
Hong KimSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.
Won-Hyuk ChoiSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.
Yu-Sub WonSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.
Bum-Joon KimSeoung-Ae Lee, Hong Kim, You-Sub Won, Bum-Joon Kim, Department of Biomedical Sciences, Microbiology and Immunology, and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-799, South Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the clinical implications of hepatitis B virus (HBV) preS1 deletion.

methodsWe developed a fluorescence resonance energy transfer-based real-time polymerase chain reaction (RT-PCR) that can detect four genotypes (wild type, 15-bp, 18-bp and 21-bp deletion). The PCR method was used in two cohorts of Korean chronic HBV subjects with genotype C infections. Cohort I included 292 chronic HBV subjects randomly selected from Cheju National University Hospital (Jeju, South Korea) or Seoul National University Hospital (Seoul, South Korea), and cohort II included 90 consecutive chronic HBV carriers recruited from Konkuk University Hospital (Seoul, South Korea); the cohort II patients did not have hepatocellular carcinoma or liver cirrhosis.

resultsThe method proposed in this study identified 341 of 382 samples (89.3%). Deletion variants were identified in 100 (29.3%) of the 341 detected samples. In both cohorts, the subjects with deletions had a significantly higher Hepatitis B virus e antigen (HBeAg)-positive seroprevalence [cohort I, wild (51.0%) vs deletion (75.0%), P < 0.001; cohort II, wild (69.2%) vs deletion (92.9%), P = 0.002] and higher HBV DNA levels [cohort I, wild (797.7 pg/mL) vs deletion (1678.9 pg/mL), P = 0.013; cohort II, wild (8.3 × 10(8) copies/mL) vs deletion (2.2 × 10(9) copies/mL), P = 0.049], compared to subjects with wild type HBV.

conclusionHBV genotype C preS1 deletion may affect disease progression in chronic HBV subjects through an extended duration of HBeAg seropositive status and increased HBV replications.

Indexed as

Gene DeletionAdultCodon, InitiatorDisease ProgressionDNA, ViralFemaleFluorescence Resonance Energy TransferGenotypeHepatitis B, ChronicHepatitis B Surface AntigensHepatitis B virusHospitals, UniversityHumansMaleMiddle AgedPhenotypeCodon, InitiatorDNA, ViralHepatitis B Surface Antigenspresurface protein 1, hepatitis B surface antigenProtein PrecursorsGenotype CHepatitis B virusHepatitis B virus e antigenHepatocellular carcinomaPreS1 start codon deletion

Identifiers

PMID25945020
PMCPMC4408479

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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.