HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplementary figures and table All Versions of this Article: vir.0.012013-0v1 vir.0.012013-0v2 90/10/2442    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Garmiri, P. Articles by Allain, J.-P. PubMed PubMed Citation Articles by Garmiri, P. Articles by Allain, J.-P. Agricola Articles by Garmiri, P. Articles by Allain, J.-P.

Deletions and recombinations in the core region of hepatitis B virus genotype E strains from asymptomatic blood donors in Guinea, west Africa

¹ Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK
² National Blood Transfusion Center, Conakry, Guinea
³ National Health Service Blood and Transplant, Cambridge Blood Centre, Cambridge, UK

Correspondence
Penelope Garmiri
pg337{at}cam.ac.uk

The prevalence of hepatitis B virus (HBV) surface antigen (HBsAg) chronic carriage in west Africa is the highest in the world, but its molecular epidemiology remains relatively poorly investigated. Plasma samples from random asymptomatic carriers of HBsAg in Conakry, Guinea, were studied and the complete genome sequences of 81 strains were obtained. Three additional samples from Kumasi, Ghana, were also included in the analysis. Phylogenetic analyses confirmed the dominance of genotype E (95.1 %), including 8.6 % of strains (viral load, 5x10³–2.6x10⁸ IU ml^–1) comprising dominant variants with large deletions in the core region and minority wild-type variants. The presence of two different patterns of deletions in two and four donors suggested targeted genome fragility between nt 1979 and 2314. The remaining sequences included one subgenotype A3 (1 %) and six A/E recombinant forms (4–7 %). A/E strains with identical points of recombination in three donors suggested strongly that these recombinant HBV strains are circulating and transmitted in the population. Recombination points were concentrated in the core gene. The detection of similar A/E recombinant strains in Ghana suggested a geographical extension of recombinant HBV to the region. The quasispecies of one additional Ghanaian strain sequenced in the pre-surface/surface region resolved into dominant clones of either the A or E genotype, but also three different patterns of A/E recombinant variants. The observation that both deletions of genotype E strains and A/E recombination points are mostly located in the core gene at specific positions indicates a region of the genome where genetic rearrangements preferentially take place.

The GenBank/EMBL/DDBJ accession numbers for the complete genome sequences are GQ161753 [GenBank] –GQ161838 [GenBank] and those for the pre-S/S clones are GQ161839 [GenBank] –GQ161846.

Two supplementary figures, showing Bayesian phylogeny of complete HBV genome sequences from Guinea or Ghana and evidence of recombination between HBV genotypes E and A or E and D in strains originating from Guinea or Ghana, and a supplementary table, listing the status of HBV markers in DEL samples from Guinean blood donors, are available with the online version of this paper.