Evidence map›Paper›PMID 41200694›Full record

ArticleOpen forum infectious diseases2025

Whole-Genome Sequencing of Hepatitis B Virus Genotypes E and A in Zambia Reveals Limited Viral Diversity in HIV Coinfection.

Michael J Vinikoor, Andreas Walker, Bright Nsokolo, Taonga Musonda, Guy Muula, Eleftherios Michailidis, Gilles Wandeler, Nadia Alatrakchi, Paul Kelly, Maximillian Damagnez and 17 more

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Open forum infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07589985 (Hep Mec Cohort in Zambia), which is not on this map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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.

NCT07589985 recruitingnot on this map

Hep Mec Cohort in Zambia

TypeobservationalSponsorUniversity of Alabama at BirminghamRan2020 to 2030Enrolled390ConditionsHepatitis B, HIV
3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
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

27 authors.

Michael J VinikoorDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Andreas WalkerInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.
Bright NsokoloSchool of Medicine, University of Zambia, Lusaka, Zambia.
Taonga MusondaSchool of Medicine, University of Zambia, Lusaka, Zambia.
Guy MuulaResearch Department, Centre for Infectious Disease Research in Zambia, Lusaka, Zambia.
Eleftherios MichailidisDepartment of Pediatrics, Emory University, Atlanta, Georgia, USA.
Gilles WandelerDepartment of Infectious Diseases, University of Bern, Bern, Switzerland.ORCID https://orcid.org/0000-0002-5278-8763
Nadia AlatrakchiDivision of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Paul KellySchool of Medicine, University of Zambia, Lusaka, Zambia.ORCID https://orcid.org/0000-0003-0844-6448
Maximillian DamagnezInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.
Duyen Bao LeInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.ORCID https://orcid.org/0009-0006-4809-938X
Anja VogesInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.
Nadine LübkeInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.ORCID https://orcid.org/0000-0003-3820-7915
Annie KanungaSchool of Medicine, University of Zambia, Lusaka, Zambia.
Samuel BosomprahResearch Department, Centre for Infectious Disease Research in Zambia, Lusaka, Zambia.ORCID https://orcid.org/0000-0002-2826-3887
Debika BhattacharyaDepartment of Medicine, University of California at Los Angeles, Los Angeles, California, USA.ORCID https://orcid.org/0000-0002-2136-7763
Carolyn ChibundiResearch Department, Centre for Infectious Disease Research in Zambia, Lusaka, Zambia.
Given BwalyaSchool of Medicine, University of Zambia, Lusaka, Zambia.ORCID https://orcid.org/0009-0008-3392-4927
Kalo Musukuma-ChifuloResearch Department, Centre for Infectious Disease Research in Zambia, Lusaka, Zambia.
Aleksei SuslovDepartment of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Martin FeuerherdDivision of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts, USA.ORCID https://orcid.org/0000-0002-5272-6503
Markus H HeimDepartment of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.ORCID https://orcid.org/0000-0002-7523-4894
Robert E SchwartzDepartment of Medicine, Cornell University, New York, New York, USA.
Raymond T ChungDivision of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Georg LauerDivision of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts, USA.ORCID https://orcid.org/0000-0002-9792-4271
Edford SinkalaSchool of Medicine, University of Zambia, Lusaka, Zambia.ORCID https://orcid.org/0000-0002-5756-5569
Jörg TimmInstitute of Virology, University of Düsseldorf, Medical Faculty, Düsseldorf, Germany.ORCID https://orcid.org/0000-0001-7799-3045

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The molecular characteristics of hepatitis B virus (HBV) in Africa, including the impact of HIV coinfection, are poorly understood. Methods: We performed whole-genome sequencing (WGS) on biospecimens collected before antiviral therapy in a well-characterized cohort of adults with HBV in Zambia, enriched for HIV coinfection (HBV/HIV). We assessed the frequency of basal core promoter (BCP) and precore variants, substitution frequencies, and the ratio of nonsynonymous to synonymous substitutions (dN/dS ratios), a surrogate for selection pressure. Results: Among 215 participants (median age, 33 years; 36% e antigen [HBeAg] positive, 35% with HBV/HIV), 114 (53.0%) had viral genotype E (gtE), and 101 (47.0%) had genotype A (gtA), subgenotype 1. BCP and precore variants, associated with HBeAg negativity, were more common with increased age, in the absence of HIV, and with gtE. Distinct from gtA, gtE had dN/dS ratios that were increased in the core vs polymerase region. Low dN/dS ratios were observed in HBV/HIV, especially at the lowest CD4 T-cell frequencies. Sequences from acute HBV infection as well as from 5 participants with chronic HBV/HIV who cleared hepatitis B surface antigen early during tenofovir-based antiretroviral therapy showed remarkably low dN/dS ratios. Conclusions: HBV gtE exhibited distinct substitution patterns compared with gtA, and HBV/HIV was associated with reduced HBV sequence diversity, consistent with impaired immune pressure.

Indexed as

hepatitis B virushuman immunodeficiency virussub-Saharan Africaviral sequencing

Identifiers

PMID41200694
PMCPMC12587420

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Registered trials

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.