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The samples were sequenced in an ABI3130XL sequencer (Applied Biosystems, Carlsbad, California, USA). Sequences were aligned with ClustalX?v1.83 [13], and edited with Bioedit?v7.0.9.0 software [14]. Phylogenetic analyses were performed using the maximum-likelihood method with tree bisection and reconnection branch swapping (PAUP* v4.0b10 [15]). The model of nucleotide substitution estimated by the Modeltest?3.7 program [16] was GTR+I+��. The robustness of the phylogenetic grouping was evaluated by a neighbor-joining bootstrap analysis with 10?000 replicates (PAUP* v.4.0b10). Quantitative variables were analysed by non-parametric tests (Mann�CWhitney), and categorical variables by chi-squared or Fisher��s exact tests. The data were stratified into 2?��?2 tables, and measures of association check details were tested. The strength of the relationship was estimated by using ORs with 95%?CIs. Multivariate analyses with logistic regression were used to determine the independent factors associated with the clinical course and the HBeAg status of the infection. Dummy variables were created for the variable ��genotype�� (with more than two classes). The Spearman correlation test was used to evaluate the related variables. Differences were considered to be significant for p-values TRIB1 were excluded from further analysis. Genotyping discrepancies between the methodologies were found in nine of the 121 sequenced samples (7.4%). The distribution of genotype?F sequences in the phylogenetic tree showed that a unique source of viruses was not supported, MK-2206 ic50 either for acute or for chronic isolates (Fig.?1). The analysis of the diversity of genotype?D isolates showed that phylogeographical relationships of Argentinean samples were not evident, dismissing the existence of a local cluster (Fig.?2). Comparative epidemiological, biochemical, virological, clinical and histological features of the studied population are shown in Tables?1 and 2. The overall prevalence of HBV genotypes in the 128 cases analysed was as follows: genotype?F, 46.9% (60/128); genotype?A, 28.1% (36/128); genotype?D, 21.9% (28/128); genotype?C, 2.3% (3/128); and genotype?B, 0.8% (1/128). A differential distribution of genotypes with regard to the clinical course of infection was found. Among the 46 acute infections, the distribution was as follows: genotype?F, 65.2% (30/46); genotype?A, 30.4% (14/46); and genotype?D, 4.3% (2/46). However, among the 82 chronically infected patients, a homogeneous distribution of genotypes?A, D and F was observed (26.8% (22/82), 31.7% (26/82) and 36.6% (30/82), respectively), as well as a few cases of genotypes?B (1.2%, 1/82) and C (3.7%, 3/82).
