Evidence map›Paper›PMID 30813638›Full record

ArticleGenes2019

High Frequency of Either Altered Pre-Core StartCodon or Weakened Kozak Sequence in the CorePromoter Region in Hepatitis B Virus A1 Strainsfrom Rwanda.

Heléne Norder, Theogene Twagirumugabe, Joanna Said, Yarong Tian, Ka-Wei Tang, Magnus Lindh

Open access · goldAbstract read
In one paragraph

Article in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

6 authors at 2 institutions in 2 countries.

Heléne NorderDepartment of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. Helene.norder@gu.se.
Theogene TwagirumugabeSchool of Medicine and Pharmacy, College of Medicine and Health Sciences, University of Rwanda, Kigali, Rwanda. twagirumugabe@gmail.com.
Joanna SaidDepartment of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. joanna.said@microbio.gu.se.
Yarong TianDepartment of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. yarong.tian@gu.se.
Ka-Wei TangDepartment of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. kawei.tang@gu.se.
Magnus LindhDepartment of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. magnus.lindh@microbio.gu.se.
University of Gothenburg · SEUniversity of Rwanda · RW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) is endemic in Rwanda and is a major etiologic agent for chronic liver disease in the country. In a previous analysis of HBV strains from Rwanda, the S genes of most strains segregated into one single clade of subgenotype, A1. More than half (55%) of the anti-HBe positive individuals were viremic. In this study, 23 complete HBV genomes and the core promoter region (CP) from 18 additional strains were sequenced. Phylogenetic analysis of complete genomes confirmed that most Rwandan strain formed a single unique clade, within subgenotype A1. Strains from 17 of 22 (77%) anti-HBe positive HBV carriers had either mutated the precore start codon (9 strains with either CUG, ACG, UUG, or AAG) or mutations in the Kozak sequence preceding the pre-core start codon (8 strains). These mutually exclusive mutations were also identified in subgenotypes A1 (70/266; 26%), A2 (12/255; 5%), and A3 (26/49; 53%) sequences from the GenBank. The results showed that previous, rarely described HBV variants, expressing little or no HBeAg, are selected in anti-HBe positive subgenotype Al carriers from Rwanda and that mutations reducing HBeAg synthesis might be unique for a particular HBV clade, not just for a specific genotype or subgenotype.

Indexed as

MutationCase-Control StudiesCodon, InitiatorHepatitis B AntibodiesHepatitis B, ChronicHepatitis B virusHumansPhylogenyPromoter Regions, GeneticRwandaViral ProteinsCodon, InitiatorHepatitis B AntibodiesViral Proteinsbasal core promoterHBVsubgenotype A1Sub-Saharan Africa

Identifiers

PMID30813638
PMCPMC6471190
OpenAlexW2918080736

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.