P36: Occupational blood exposure and compliance to universal precautions: a cross‐sectional survey among healthcare workers in Beijing, China

Abstract

PURPOSE OF THE STUDY: The goals of our study were to evaluate HBV genotypes and recombinants; mutations related to antiviral resistance, hepatic disease progression and vaccine escape in HBV monoinfected patients in S~ ao Paulo city, Brazil. METHODS: Full-length or partial HBV sequences from 39 treated and untreated patients were performed (1). Mutations were mapped and phylogenetic analyses performed. RESULTS: Twenty-eight full-length and 11 partial HBV sequences (HBsAg and the RT domain) were obtained. The genotype distribution was: A (51.3%), D (25.6%), F (15.4%) and C (7.7%). Primary resistance mutations were not found, however, we found compensatory mutations in 43% of the treated patients and 12.5% among untreated patients. We also found mutations related to changes in the HBsAg antigenicity (vaccine escape and decrease of HBsAg detection in serological tests); disease progression in the precore/core gene (85.7%), including A1762T/ G1764A/G1896A mutations in HBsAg positive and negative patients; and deletions in the Pre-S1 and Pre-S2 region (14%), more specifically in the start codons and the S gene promoter. CONCLUSIONS: The genotype distribution (A, D, F and C) reflects the historical context of the population from S~ ao Paulo, which is composed of immigrants from Africa (A), Europe (D) and Asia (C), and migrants, mostly coming from the Northeast (A) and North of Brazil (F), being the Amerindian population common in the North region. Most of the S gene mutations, which lead to the HBsAg antigenicity changes, are the characteristics that distinguish the different genotypes, which might explain the antigenicity differences among them. A1762T/G1764A/G1896A mutations in the core/precore region are not common in HBeAg positive patients, and G1896A mutation is not common in genotypes A and F either, but it was found in this study. In the analysis of the nucleotide 1858 in the two sequences with G1896A mutation, genotypes A and F respectively, T1858 was found instead of C1858, which would allow the selection of the G1896A mutation in these genotypes. The Pre-S deletions in start codons and A1762T/G1764A/G1896A mutations in positive HBeAg patients may be related to non-majoritary viral populations and need further studies using next-generation sequencing technologies. REFERENCE