Evidence map›Paper›PMID 25100867›Full record

ArticleClinical infectious diseases : an official publication of the Infectious Diseases Society of America2014

Hepatitis B virus sub-genotype A1 infection is characterized by high replication levels and rapid emergence of drug resistance in HIV-positive adults receiving first-line antiretroviral therapy in Malawi.

Samir Aoudjane, Mas Chaponda, Antonio Adrián González Del Castillo, Jemma O'Connor, Marc Noguera, Apostolos Beloukas, Mark Hopkins, Saye Khoo, Joep J van Oosterhout, Anna Maria Geretti

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Article in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 4 pooled it
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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

18 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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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

10 authors.

Samir AoudjaneDivision of Infection & Immunity and London Centre for Nanotechnology.
Mas ChapondaDepartment of Infectious Diseases, University of Liverpool/Malawi Liverpool Wellcome Trust, United Kingdom.
Antonio Adrián González Del CastilloDivision of Infection & Immunity and London Centre for Nanotechnology.
Jemma O'ConnorDepartment of Infection & Population Health, University College London.
Marc NogueraIrsiCaixa & AIDS Unit, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain.
Apostolos BeloukasInstitute of Infection and Global Health.
Mark HopkinsDepartment of Virology.
Saye KhooInstitute of Translational Medicine, University of Liverpool, United Kingdom.
Joep J van OosterhoutCollege of Medicine, University of Malawi, Blantyre Dignitas International, Zomba, Malawi.
Anna Maria GerettiInstitute of Infection and Global Health.

Funding

Wellcome Trust 100890
6 · The paper itself

Abstract

backgroundIt has been proposed that hepatitis B virus (HBV) sub-genotype A1 infections have mild outcomes and a low risk of drug-resistance among patients infected with human immunodeficiency virus (HIV) receiving lamivudine-containing antiretroviral therapy (ART) without tenofovir in Africa.

methodsThe virologic expression of HBV sub-genotype A1 coinfection was studied over 12 months in HIV-positive adults starting stavudine/lamivudine/nevirapine in Malawi, using Sanger, deep, clonal, and single full-genome sequencing for the sensitive characterization of HBV resistance-associated mutations (RAMs).

resultsAmong 1117 subjects, 133 (12%) tested HBsAg-positive. After starting ART, retention rates were 96/133 (72%) at 6 months and 54/133 (41%) at 12 months. Based upon the last available follow-up, 92/96 (96%) subjects achieved HIV-1 RNA <40 copies/mL, 48/96 (50%) showed HBV DNA <14 IU/mL, and 24/96 (25%) acquired HBV RAMs. At 6 months, M204I was detected in 8/46 (17%) and 16/17 (94%) subjects using Sanger and deep sequencing, respectively. At 12 months, all viremic patients had multiple resistance and compensatory mutations coexisting on the same HBV genomes. Comparing HBeA-positive (67/133, 50%) with HBeAg-negative subjects, 64/67 (96%) vs 35/66 (55%) showed baseline HBV DNA >2000 IU/mL (P = .0006), 39/47 (17%) vs 9/49 (82%) had persistent HBV DNA detection during follow-up (P < .0001), and 23/47 (49%) vs 2/49 (4%) acquired HBV RAMs (P < .0001). Baseline HBV DNA levels were median 8.1 vs 5.3 log10 IU/mL in subjects with vs those without treatment-emergent RAMs (P < .0001).

conclusionsHBV sub-genotype A1 infections showed a severe virologic expression in HIV-positive Malawians. The findings strengthen the urgency of interventions to improve ascertainment and management of chronic hepatitis B in the region.

Indexed as

AdultAnti-HIV AgentsDNA, ViralDrug Resistance, ViralFemaleHepatitis BHepatitis B virusHIV InfectionsHumansLamivudineMalawiMaleNevirapinePhylogenyRetrospective StudiesSequence Analysis, DNAAnti-HIV AgentsDNA, ViralLamivudineNevirapineStavudinestavudine, lamivudine, nevirapine drug combinationAfricalamivudineresistancesub-genotype A1viral load

Identifiers

PMID25100867
PMCPMC4650769

What OpenQuestion holds

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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.