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Genes (Basel). 2019 Feb 26;10(3). pii: E182. doi: 10.3390/genes10030182.

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

Author information

1
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. Helene.norder@gu.se.
2
School of Medicine and Pharmacy, College of Medicine and Health Sciences, University of Rwanda, Kigali, Rwanda. twagirumugabe@gmail.com.
3
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. joanna.said@microbio.gu.se.
4
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. yarong.tian@gu.se.
5
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. kawei.tang@gu.se.
6
Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 405 30 Gothenburg, Sweden. magnus.lindh@microbio.gu.se.

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.

KEYWORDS:

HBV; Sub-Saharan Africa; basal core promoter; subgenotype A1

Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

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