Distribution of Hepatitis B Virus Genotypes in Two Different Pediatric Populations from Argentina

Abstract

Differences in pathogenesis and the probability of becoming a chronic carrier depend on the age at which hepatitis B virus (HBV) infection is acquired, ranging from 82% in infants less than 6 months of age to 15 to 30% in older children. HBV genotypes from 22 pediatric patients from two areas that differ in prevalence have been determined. Phylogenetic analysis shows a clear difference between the genotype distribution in Buenos Aires, a low-prevalence area, and that found in Gualeguay, Entre Rı́os, a high-prevalence area. While the analysis allocated the sequences in the Buenos Aires group to genotypes A (36%), D (9%), and F (55%), the Gualeguay group presented exclusively genotype A isolates with very low nucleotide divergence, which suggests a strong founder viral population. The high prevalence of genotype F in the Buenos Aires group and its high intragroup heterogeneity agree with the American origin of this genotype.

Phylogenetic analysis of new hepatitis B virus isolates from Nigeria supports endemicity of genotype E in West Africa*

“…Other researchers [Bowyer and Sim, 2000] showed that members of genotypes A, B, C, and D are diverse enough to justify classi®cation into subgroups with inter-subgroup divergence of up to 4%. This high level of intragenotypic diversity, even among isolates found within the same city [Bowyer et al, 1997;Mbayed et al, 1998], has been interpreted as an indication of endemicity and a long natural history of these genotypes within their human hosts. In our isolates, combined with earlier genotype E isolates, the diversity of genotype E reached only 1.5%.…”

Genotype and Subtype Analyses of Hepatitis B Virus (HBV) and Possible Co‐Infection of HBV and Hepatitis C Virus (HCV) or Hepatitis D Virus (HDV) in Blood Donors, Patients with Chronic Liver Disease and Patients on Hemodialysis in Surabaya, Indonesia

“…In brief, HBV DNA extracted from sera by a phenol-chloroform method was subjected to PCR over 35 cycles, with each cycle consisting of 1 min at 94 C, 1 min at 55 C, and 2 min at 72 C, to amplify part of the surface gene using primers P7 (5'-GTGGTGGACTTCTCTCAATTTTC-3', positions 256 to 278) and P8 (5'-CGGTAWAAAGGGACTCAM-GAT-3', positions 796 to 776) (14). If the first-round PCR amplification was negative, the second-round PCR was performed using primers HBS1 (5'-CAAGGTAT-GTTGCCCGTTTG-3', positions 455 to 474) and HBS2 (5'-AAAGCCCTGCGAACCACTGA-3', positions 713 to 694) (19,38,42) under the same condition described above. Nucleotide sequences of the amplified fragments were determined with the Big Dye Deoxy Terminator Cycle Sequencing kit (Perkin Elmer) and ABI377 or ABI310 DNA sequencer (Applied Biosystem, Inc.), and amino acid sequences were deduced.…”

Hepatitis B virus genotypes, subgenotypes, precore, and basal core promoter mutations in the two largest provinces of Pakistan

“…[1][2][3] Certain type of infectious agents are harbored in specific areas or communities, therefore typing the infectious agent can provide very important information in studying not only the spreading pattern of the agent itself, but also the migration pattern of humans. [4][5][6] Genotypes can influence the course of viral disease and give rise to genotypic-specific biological differences, 6 such as help in monitoring the efficacy of treatment pattern, classifying the route and pathogenesis of virus, 7 severity of disease, HBeAg seroconversion rates, precore and core promoter mutation patterns, 8 and the development of resistance to antiviral therapy. 9 It has also been reported that specific viral sequence determination before the commencement of therapy can help in predicting the long-term response to therapy.…”