Evidence map›Paper›PMID 27482430›Full record

ArticleJournal of virus eradication2016

Hepatitis B virus genotypes A and D in Uganda.

Jackie T Zirabamuzale, Christopher K Opio, Freddie Bwanga, Emmanuel Seremba, Betty S Apica, Robert Colebunders, Ponsiano Ocama

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Article in Journal of virus eradication, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Article
  4. Article
  5. Article
  6. 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

7 authors.

Jackie T ZirabamuzaleDepartment of Medicine , Makerere University College of Health Sciences, Mulago Hospital , Kampala , Uganda.
Christopher K OpioDepartment of Medicine , Makerere University College of Health Sciences, Mulago Hospital , Kampala , Uganda.
Freddie BwangaDepartment of Microbiology , Makerere University College of Health Sciences , Kampala , Uganda.
Emmanuel SerembaDepartment of Medicine , Makerere University College of Health Sciences, Mulago Hospital , Kampala , Uganda.
Betty S ApicaDepartment of Medicine , Makerere University College of Health Sciences, Mulago Hospital , Kampala , Uganda.
Robert ColebundersInstitute of Tropical Medicine , University of Antwerp , Belgium.
Ponsiano OcamaDepartment of Medicine , Makerere University College of Health Sciences, Mulago Hospital , Kampala , Uganda.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe prevalence of hepatitis B virus (HBV) infection in Uganda is 10%. Hepatitis B virus genotypes impact on treatment response, rate of spontaneous recovery and progression of chronic HBV infection and hepatocellular carcinoma. There is little information on the HBV genotypic distribution in Uganda.

objectivesTo determine HBV genotypes in Uganda.

methodsThe MBN clinical laboratory performs HBV viral load and genotype testing in Uganda. It receives hepatitis B surface antigen (HBsAg)-positive samples from all over the country for additional HBV testing. Samples are stored for 6 months before being discarded. Our study used delinked stored samples. PCR-positive samples had DNA extracted and used as template for HBV genome amplification by nested PCR. Reverse hybridisation was performed and genotypes were determined by the line probe assay method (INNO-LiPA).

resultsOne hundred stored HBsAg-positive plasma samples with detectable viral loads were analysed. Of these, 93 samples showed PCR amplification products and gave genotype-specific probe lines on the INNO-LiPA assay. Of the patients, where gender was recorded, 60.9% were female, and the overall median age (IQR) was 25 (2-60) years. There was a predominance of HBV genotype D (47 patients; 50.5%), followed by genotype A, (16 patients; 17.2%). One patient (1.1%) had genotype E. In 28% of the samples mixed infections were detected with genotypes A/E (9.7%) and A/D (6.5%) being most common. Genotypes B, C, E and H only occurred as part of mixed infections.

conclusionHepatitis B genotypes D and A were predominant in our study population.

Identifiers

PMID27482430
PMCPMC4946690

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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.