Dados do Trabalho

Título

GENETIC DIVERSITY OF HEPATITIS B VIRUS IN ACUTE AND DIFFERENT STAGES OF CHRONIC INFECTION

Introdução

The selection pressure imposed by the host immune system impacts hepatitis B virus (HBV) genetic variability.

Objetivo(s)

This study evaluates HBV genetic diversity, nucleos(t)ide analogs (NA) resistance and HBsAg escape mutations in HBV patients according to phases of chronic hepatitis B infection (CHB) and HIV status.

Material e Métodos

A total of 106 HBsAg+ patients over 18 years of age were included. Four different phases of CHB were included: 12 immune tolerant (IT), 8 immune reactive HBeAg¬ positive (IR), 46 low replicative (LR), 24 HBeAg-negative CHB (ENH) phases. In addition, 13 acute-infected and 9 HIV/ HBV coinfected individuals were included. Samples were PCR amplified and sequenced for the overlapping POL/S region. Phylogenetic analyses were performed using Mega-X software. Identification of vaccine escape and resistance mutations was performed using the Geno2Pheno HBV website.

Resultados e Conclusão

Mean age was 44.5± 13.3 years and most of subjects were males (56.9%). Most of the individuals presented genotype A (75.3%), subgenotype A1 (61 3%), irrespective of group, followed by genotypes D (17.3%), F (6.4%) and E (1.1%). Genotypes D and F were more prevalent in LR group (75% and 66.6%, respectively) and genotype E was found only in IT group (1/1). No antiviral resistance mutation was observed. However, high frequency of HBsAg mutations was found in all groups, such as, M129L (72.0%); W1 53RW (36 5%); V1 63I (64.5%); I253V (55.9%); V278IV (30.1%). Seven subjects (7.5%) presented HBsAg escape mutations, most of them are genotype A infected (85.7%) and belongs to LR group (57.1%); 1 is genotype D infected (14.3%), 2 were HIV/ HBV coinfected (28.6%) and 1 was ENH (14.3%). It was found a high prevalence of genotype A1 irrespective of CHB phase or HIV coinfection. HBsAg escape mutations were detected in treatment-naive patients and could impact antiviral treatment and diagnosis.

Palavras-chave

HBV, genotypes, chronic infection, genetic variability