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Maternofetal transmission of hepatitis B virus genotype E in Ghana, west Africa

¹ National Health Service Blood and Transplant, Cambridge Blood Centre, Cambridge, UK
² Department of Obstetrics and Gynaecology, Komfo Anokye Teaching Hospital, Kumasi, Ghana
³ Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK

Correspondence
Daniel Candotti
dc241{at}cam.ac.uk

To determine whether maternofetal transmission of hepatitis B virus (HBV) is a common route of infection leading to chronic infection in west Africa, plasma samples, obtained at delivery from 1368 pregnant Ghanaian women and paired umbilical cord blood or newborn whole blood samples, were tested for HBV surface antigen (HBsAg) and DNA. A 16 % prevalence of HBV chronic carriers, defined as detectable HBsAg and/or HBV DNA, was found, >80 % contained less than 1x10⁴ IU ml^–1 HBV DNA and 99 % were infected with genotype E strains. HBV maternofetal transmission was documented in 17 out of 204 (8.3 %) paired HBV carrier women–cord blood/newborn samples. The rate of transmission was 55 % and 3.3 % when maternal viral load was above or below 1x10⁴ IU ml^–1, respectively (P=0.0008). Maternofetal transmission of HBV genotype E was estimated to account for 8 % of the cases of chronic HBsAg carriers. Six women with low viral load at delivery (five <20 IU ml^–1) and anti-HBe (hepatitis B e antigen) transmitted HBV. Surprisingly, while non-transmitted low viral load strains had 79 % mutations at position 1896 of HBV genome, transmitted strains were all wild-type despite anti-HBe presence (P=0.0041), suggesting the possible role of HBeAg as risk factor for HBV maternofetal transmission. The relative risk of maternofetal transmission was 2.4 when pregnant women carried high viral load and 11.5 when carrying wild-type strains at position 1896, irrespective of viral load. We conclude that viral load and pre-core wild-type at position 1896 are two independent risk factors for HBV genotype E maternofetal transmission, which remains a minor contributor to high prevalence of chronic infection.

The GenBank/ENBL/DDBJ accession numbers for the sequences determined in this study are EF655914–EF655977 and EF661996–EF662052.