Evidence map›Paper›PMID 39986372›Full record

ArticleAnnals of hepatology

A putative hepatitis B virus sequence motif associated with hepatocellular carcinoma in South African adults.

Tongai G Maponga, Anna L McNaughton, Cori Campbell, Mariateresa de Cesare, Jolynne Mokaya, Sheila F Lumley, David Bonsall, Camilla Lc Ip, Haiting Chai, Christo Van Rensburg and 8 more

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of hepatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Tongai G MapongaDivision of Medical Virology, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg, Cape Town, South Africa; National Health Laboratory Service, Tygerberg Business Unit, Tygerberg, Cape Town, South Africa.
Anna L McNaughtonNuffield Department of Medicine, University of Oxford, Oxford, UK.
Cori CampbellNuffield Department of Medicine, University of Oxford, Oxford, UK.
Mariateresa de CesareNuffield Department of Medicine, University of Oxford, Oxford, UK.
Jolynne MokayaParasites and Microbes, Wellcome Sanger Institute, Hinxton, UK.
Sheila F LumleyNuffield Department of Medicine, University of Oxford, Oxford, UK; Department of Infectious Diseases and Microbiology, Oxford University Hospitals NHS Foundation Trust, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
David BonsallNuffield Department of Medicine, University of Oxford, Oxford, UK; Department of Infectious Diseases and Microbiology, Oxford University Hospitals NHS Foundation Trust, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK; Big Data Institute, Old Road, Oxford OX3 7FZ, UK.
Camilla Lc IpNuffield Department of Medicine, University of Oxford, Oxford, UK.
Haiting ChaiNuffield Department of Medicine, University of Oxford, Oxford, UK.
Christo Van RensburgDivision of Gastroenterology, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg, Cape Town, South Africa.
Richard H GlashoffNational Health Laboratory Service, Tygerberg Business Unit, Tygerberg, Cape Town, South Africa; Immunology Unit, Division of Medical Microbiology, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg, Cape Town, South Africa.
Elizabeth WaddiloveThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.
Wolfgang PreiserDivision of Medical Virology, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg, Cape Town, South Africa; National Health Laboratory Service, Tygerberg Business Unit, Tygerberg, Cape Town, South Africa.
Jason T BlackardUniversity of Cincinnati College of Medicine, Cincinnati, OH, USA.
M Azim AnsariNuffield Department of Medicine, University of Oxford, Oxford, UK.
Anna KramvisHepatitis Virus Diversity Research Unit, Department of Internal Medicine, University of the Witwatersrand, 7 York Road, Parktown, 2193 Johannesburg, South Africa.
Monique I AnderssonDivision of Medical Virology, Stellenbosch University, Faculty of Medicine and Health Sciences, Tygerberg, Cape Town, South Africa; Nuffield Department of Medicine, University of Oxford, Oxford, UK; Department of Infectious Diseases and Microbiology, Oxford University Hospitals NHS Foundation Trust, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK.
Philippa C MatthewsThe Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK; Division of Infection and Immunity, University College London, Gower Street, London WC1E 6BT, UK; Department of Infectious Diseases, University College London Hospital, Euston Road, London NW1 2BU, UK. Electronic address: philippa.matthews@crick.ac.uk.

Funding

Columbia-South Africa Training Program for Research on HIV-associated MalignanciD43CA153715 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI NEUGUT, ALFRED I. · 2010 to 2013
$1.8M
NCI NIH HHS D43 CA153715Wellcome Trust CC2223
6 · The paper itself

Abstract

INTRODUCTION AND

objectivesChronic hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC). In African populations, HCC frequently presents at an advanced stage with poor outcomes. We applied whole genome sequencing (WGS) to compare HBV genomes in individuals with and without HCC. MATERIALS AND

methodsWe identified adults with HBV infection, with and without complicating HCC, in Cape Town, South Africa. We generated HBV WGS using pan-genotypic probe-based enrichment followed by Illumina sequencing.

resultsCompared to the non-HCC group, HCC patients were more likely to be male (p < 0.0001), older (p = 0.01), HIV-negative (p = 0.006), and have higher HBV viral loads (p < 0.0001). Among 19 HCC and 12 non-HCC patients for whom WGS was obtained, genotype A dominated (74 %), of which 96 % were subgenotype A1. PreS2 deletions (Δ38-55) were enriched in HBV sequences from HCC patients (n = 7). The sequence motif most strongly associated with HCC comprised either a deletion or polymorphism at site T53 in PreS2 - collectively coined 'non-T53' - together with a basal core promoter (BCP) mutation G1764A (AUROC = 0.79).

conclusionsIn this setting, HBV sequence polymorphisms and deletions are associated with HCC, and 'non-T53 + G1764A' represents a putative signature motif for HCC. Additional investigations are needed to disaggregate the impact of other demographic, clinical, and environmental influences, to ascertain the extent to which viral polymorphisms contribute to oncogenesis, and to determine whether HBV sequence is a useful biomarker for HCC risk stratification.

Indexed as

Carcinoma, HepatocellularDNA, ViralHepatitis B, ChronicHepatitis B virusLiver NeoplasmsGenome, ViralGenotypeHepatitis B Surface AntigensHumansRisk FactorsSouth AfricaViral LoadWhole Genome SequencingDNA, ViralHepatitis B Surface AntigensAfricaHepatitis B virusHepatocellular carcinomaLiver cancerWhole genome sequencing

Identifiers

PMID39986372
PMCPMC7619346

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.