Abstract
BackgroundAlthough hepatitis B virus (HBV) is hyperendemic and heterogeneous in its genetic diversity in Ethiopia, little is known about hepatitis D virus (HDV) circulating genotypes and molecular diversity.MethodsA total of 321 hepatitis B surface antigen (HBsAg) positives (125 HIV co-infected, 102 liver disease patients and 94 blood donors) were screened for anti-HDV antibody. The anti-HDV positive sera were subjected to Real time PCR for HDV-RNA confirmation. The non coding genome region (spanning from 467 to 834 nucleotides) commonly used for HDV genotyping as well as complete HDV genome were sequenced for genotyping and molecular analysis.ResultsThe anti-HDV antibody was found to be 3.2% (3) in blood donors, 8.0% (10) in HIV co-infected individuals and 12.7% (13) in liver disease patients. None of the HIV co-infected patients who revealed HBV lamivudine (3TC) resistance at tyrosine-methionine/isoleucine-aspartate-aspartate (YM(I)DD) reverse transcriptase (RT) motif with concomitant vaccine escape gene mutants was positive for anti-HDV antibody. The HDV viremia rate was 33.3%, 30.0% and 23.1% in respect to the above study groups. All the six isolates sequenced were phylogenetically classified as HDV genotype 1 (HDV-1) and grouped into two monophyletic clusters. Amino acid (aa) residues analysis of clathrin heavy chain (CHC) domain and the isoprenylation signal site (Py) at 19 carboxyl (C)-terminal amino acids (aa 196–214) and the HDV RNA binding domain (aa 79–107) were highly conserved and showed a very little nucleotide variations. All the sequenced isolates showed serine at amino acid position 202. The RNA editing targets of the anti-genomic HDV RNA (nt1012) and its corresponding genomic RNA (nt 580) showed nucleotides A and C, respectively.ConclusionsThe low seroprevalence and viraemic rates of HDV in particular during HIV-confection might be highly affected by HBV drug resistance selected HBsAg mutant variants in this setting, although HDV-1 sequences analysis revealed clade homogeneity and highly conserved structural and functional domains. Thus, the potential role of HBV drug resistance associated polymerase mutations and concomitant HBsAg protein variability on HDV viral assembly, secretion and infectivity needs further investigation.
Highlights
Hepatitis B virus (HBV) is hyperendemic and heterogeneous in its genetic diversity in Ethiopia, little is known about hepatitis D virus (HDV) circulating genotypes and molecular diversity
Patients (n = 252) in northwest Ethiopia. Among this total study population, 340 hepatitis B surface antigen (HBsAg) positive sera were studied before to determine clinically important hepatitis B virus (HBV) drug resistant and immune escape HBsAg gene variants among human immunodeficiency virus (HIV) co-infected and HBV monoinfected Ethiopians [14]. In this cross-sectional study, from the above well characterized HBsAg positive sera, 321 of them were screened for anti-HDV antibody with the proportions of blood donors (n = 94), chronic liver disease (CLD) patients (n = 102) and HIV co-infected patients (n = 125)
Exclusion of anti-HDV seroprevalence report from HBsAg negatives as the result of occult HBV infections and /or anti-HBc positive cases was the limitation of the current study
Summary
Hepatitis B virus (HBV) is hyperendemic and heterogeneous in its genetic diversity in Ethiopia, little is known about hepatitis D virus (HDV) circulating genotypes and molecular diversity. Its genome is a circular, negative sense, and single-stranded RNA of approximately 1.7 kb in length [1].The HDV anti-genome contains a unique open reading frame that encodes the Belyhun et al Virology Journal (2017) 14:176 the globally estimated 350 million HBsAg carriers, 15 to 20 million people are infected with HDV which is associated with a severe form of viral hepatitis [6]. The mechanism of HDV pathogenesis has not been fully explained [3], the severity of liver disease due to HDV varies by the nature of its co-or super-infection with HBV and as well the genotypes of both viruses [7]. The co-infection of HBV with HDV leads to acute hepatitis, but subsequent chronic infection is rare, whereas the super-infection of HDV in HBV carriers typically induces a severe form of hepatitis and causes chronic infection compared to HBV monoinfection [3]. Whether combinations of HBV genotypes with HDV genotypes cause varying clinical outcomes, remains to be explored [8, 10]
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