PreS deletions and / or mutations in hepatitis B virus (HBV) DNA from chronically infected patients (CHB): first report from Argentina.

TRINKS J; FRIAS S; ALESSIO A; PEREZ TAMBINI H; POZZATI M; BATALLA V; DALEOSO G; LEON L; HEINRICH M; MALARINO S; DIAZ A; MINASSIAN ML; ANDREETTA AM; FRIDER B; AMEIGEIRAS BM; OUBIÑA JR

Buenos Aires.

Simposio; III International Clinical Virology Simposium and Advances in Vaccines.; 2010

Pan American Society of Virology.

Background and Aims: Eight genotypes of HBV have been identified (A-H) and 2 more have been proposed (I-J). It is suggested that PreS deletions and nucleotide substitutions at the promoter sites of PreS1 and/or PreS2 may serve as useful biomarkers for predicting the clinical outcomes of HBV-infected patients, especially hepatocellular carcinoma. The aims of this study were to retrospectively assess the prevalence of PreS deletions and promoter mutations and their association with genotypes in Argentinean patients with CHB. Methods: Serum samples and epidemiological data were collected from 28 CHB patients living in Buenos Aires city (BA) and its suburbs (n = 20) or in the city of Gualeguay, Entre Ríos province (n = 8). Mean patients´age from BA (85% male) was 37.5 years ± 13.11 and 20.5 years ± 1.6 for those from Gualeguay (75% male). All samples were tested for HBV serologic markers. Hemi-nested PCR for the PreS1/PreS2/S DNA region was carried out. Different sized amplicons were purified. Genotype assignment was done by phylogenetic analysis (PHYLIP 3.5c). Epidat 3.1 software was used for statistical analysis. Results: No statistically significant differences were observed when genotype assignment and geographical location were studied. Thirteen samples were ascribed to HBV genotype A (46.4%), 12 to HBV genotype F (42.8%), 2 to genotype D (7.2%), and the remaining one corresponded to a mixed A-F infection (3.6%). The presence of PreS deletions was observed in 3 samples assigned to genotype F (25%) and 2 to genotype A (15.4%). Only 2 samples showed nucleotide substitutions at the PreS2 promoter site, both ascribed to genotype A (15.4%). Conclusions: a) unexpectedly, HBV genotype distribution was similar among patients from BA and Gualeguay (Mbayed et al., 1998); b) a significant high prevalence of PreS deletions was observed among genotype F -and to a lesser extent, genotype A- infected patients as compared with published reports; and c) PreS2 promoter mutations were only detected in a subset of genotype A cases.