Evidence map›Paper›PMID 29411271›Full record

ArticleVirus genes2018

Molecular characterization of hepatitis B virus X gene in HIV-positive South Africans.

Maemu P Gededzha, Tsakani H Sondlane, Lesibana A Malinga, Rosemary J Burnett, Ramokone L Lebelo, Jason T Blackard, M Jeffrey Mphahlele, Selokela G Selabe

Abstract read
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In one paragraph

Article in Virus genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Trial
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

8 authors at 3 institutions in 2 countries.

Maemu P GededzhaHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Tsakani H SondlaneHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Lesibana A MalingaHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Rosemary J BurnettHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Ramokone L LebeloHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Jason T BlackardDivision of Digestive Diseases, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
M Jeffrey MphahleleHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa.
Selokela G SelabeHIV and Hepatitis Research Unit, Department of Virology, Sefako Makgatho Health Sciences University and National Health Laboratory Service, P.O. Box 173, MEDUNSA, 0204, Pretoria, South Africa. selokela.selabe@smu.ac.za.
National Health Laboratory Service · ZASefako Makgatho Health Sciences University · ZAUniversity of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is a major public health problem worldwide and the major cause of hepatocellular carcinoma (HCC) in South Africa. The role of HBV in HCC is not well understood, although the HBV X gene has been implicated as a critical factor. Data on the HBV X gene in HIV-positive South Africans are limited; thus, we investigated X gene variability in 24 HIV-infected treatment-naïve patients at Dr George Mukhari Academic Hospital. Quantitative and qualitative HBV DNA tests were conducted using real-time and in-house polymerase chain reaction (PCR) assays, respectively, targeting the complete HBV X gene. In-house PCR-positive samples were cloned using the P-Gem T-easy vector System II and sequenced. By phylogenetic analysis, X gene sequences were classified as subgenotype A1 (n = 15), A2 (n = 4), and D1 (n = 4), and one dual infection with subgenotypes as A1 and C. The basal core promoter mutations T1753C, A1762T, and G1764A were identified in the majority of sequences. Genotype D sequences had a 6-nucleotide insertion. In conclusion, subgenotype A1 was predominant, and a rare dual infection of HBV genotype A and C was detected. The 6-nucleotide insertion could represent a unique variant in the region and highlights the need for functional studies of HBV X gene variants, particularly from resource-limited settings.

Indexed as

Genetic VariationCluster AnalysisGenotypeHepatitis B, ChronicHepatitis B virusHIV InfectionsHospitalsHumansMutationPhylogenyPolymerase Chain ReactionPromoter Regions, GeneticSequence Analysis, DNASequence HomologySouth AfricaTrans-Activatorshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory ProteinsAfricaGenotypeHBxHepatitis B virus (HBV)HIVSouth Africa

Identifiers

PMID29411271
OpenAlexW2791648129

What OpenQuestion holds

Textmetadata
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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.