Abstract
Hepatitis B virus genotype E (HBV/E) is highly prevalent in Western Africa. In this work, 30 HBV/E isolates from HBsAg positive Angolans (staff and visitors of a private hospital in Luanda) were genetically characterized: 16 of them were completely sequenced and the pre-S/S sequences of the remaining 14 were determined. A high proportion (12/30, 40%) of subjects tested positive for both HBsAg and anti-HBs markers. Deduced amino acid sequences revealed the existence of specific substitutions and deletions in the B- and T-cell epitopes of the surface antigen (pre-S1- and pre-S2 regions) of the virus isolates derived from 8/12 individuals with concurrent HBsAg/anti-HBs. Phylogenetic analysis performed with 231 HBV/E full-length sequences, including 16 from this study, showed that all isolates from Angola, Namibia and the Democratic Republic of Congo (n = 28) clustered in a separate lineage, divergent from the HBV/E isolates from nine other African countries, namely Cameroon, Central African Republic, Côte d'Ivoire, Ghana, Guinea, Madagascar, Niger, Nigeria and Sudan, with a Bayesian posterior probability of 1. Five specific mutations, namely small S protein T57I, polymerase Q177H, G245W and M612L, and X protein V30L, were observed in 79-96% of the isolates of the separate lineage, compared to a frequency of 0–12% among the other HBV/E African isolates.
Highlights
Hepatitis B virus (HBV) infection still remains an important cause of morbidity and mortality worldwide, in the Asian and African developing countries
We investigated the genetic diversity of Angolan Hepatitis B virus genotype E (HBV/E) isolates and demonstrate the existence of a separate cluster within genotype E formed by isolates from Angola, Namibia and the Democratic Republic of Congo
No nucleotide sequence could be determined for five of the 35 Angolan virus isolates previously characterized as HBV/E, due to insufficient amounts of PCR products
Summary
Hepatitis B virus (HBV) infection still remains an important cause of morbidity and mortality worldwide, in the Asian and African developing countries. HBV has a DNA genome of about 3.2 kb, which contains four open reading frames, namely S (surface antigen), P (polymerase), C (core protein) and X (regulatory protein). The development of antibodies against hepatitis B surface antigen (HBsAg) leads to the viral clearance. Studies performed with HBV carriers testing positive for both serological markers have demonstrated that mutations in the pre-S [6,7] and S [8,9] regions of the genome may lead to changes in the immunogenicity of the viral particles, influencing the viral behavior and clinical course of the liver disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
