Analysis of near full-length genome sequences of HIV type 1 BF intersubtype recombinant viruses from Brazil reveals their independent origins and their lack of relationship to CRF12_BF.
ABSTRACT We analyze the recombinant structures and phylogenetic relationships of nine near full-length genome sequences of HIV-1 BF intersubtype recombinant viruses from Brazil, eight of them newly derived. These were obtained by PCR amplification from peripheral blood mononuclear cells (PBMCs) DNA or PBMCs culture supernantant RNA. The recombinants exhibited unique mosaic structures, except two viruses with a single near coincident breakpoint. Comparison with CRF12_BF revealed only two coincident breakpoints in two recombinants. Phylogenetic analyses failed to support a common ancestry of Brazilian recombinants or their relationship to CRF12_BF, which widely circulates in Argentina. Intersubtype breakpoint distribution along the genome was uneven, with the highest mean frequency in the polymerase domain of reverse transcriptase, and the lowest in env. These results indicate that HIV-1 BF recombinants from Brazil have independent origins and are unrelated to CRF12_BF, and that intersubtype breakpoints are frequent in pol segments analyzed for drug resistance detection.
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- "Phylogenetic analysis of previously characterised B/F recombinant HIV-1 sequences showed that all of the sequences of the 13 subjects grouped in the same cluster as B/F recombinant sequences of various South American origins, and showed a close relationship with South American CRF12_BF [Foglieni et al., 2010]. Two recently described BF URFs from Luxemburg and Brazil (accession numbers EU170145 and AY455780 [Thomson et al., 2004]) were the closest to this strain. All of the sequences have been deposited in GenBank under accession numbers HQ834729-HQ834742. "
ABSTRACT: Migratory processes have caused changes in human immunodeficiency virus (HIV) epidemiology and non-B subtypes are now playing an increasing role. In a cohort of 553 HIV-infected outpatients tested to identify non-B isolates, the largest group consisted of 13 subjects with a recombinant B/F form (prevalence 2.4%). Sequencing and phylogenetic analyses described a B/F recombinant clade with anomalous breakpoints that did not allow it to be classified as CRF12_BF. Viral load was not quantified efficiently because of a mismatch in the primers and probes used by commercial assays. An assessment of the clinical management, and epidemiological, immunological, and virological characteristics of these patients, who were receiving non-nucleoside reverse transcriptase inhibitor (NNRTI)- or protease inhibitor (PI)-based regimens, showed that the immunological and virological mismatch delayed the start of treatment by a mean of 6.8 months. Therapy was started in nine patients. Both NNRTI- and PI-based regimens led to full virological suppression after a mean 36 weeks of treatment; the PI-based regimens proved to be more effective in terms of immunological recovery (1,341 vs. 544 CD4+ cells/mm(3) ). The spread of non-B subtypes is increasing throughout the world but their response to treatment is still unclear. PIs and NNRTIs are effective but further tests are needed to allow the more efficient recognition of these viral strains and establish how they should be treated.Journal of Medical Virology 09/2011; 83(9):1493-8. DOI:10.1002/jmv.22142 · 2.22 Impact Factor
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- "All HIV-1 subtype classification in this study refers solely to the PR region. Some nucleotide sequences used in the analyses were previously determined experimentally and had their subtype assigned by our group and others (Vicente et al., 2000; Caride et al., 2001; Brindeiro et al., 2002, 2003; E.A. Soares et al., 2003; M.A. Soares et al., 2003; Soares et al., 2005, 2007 ; Dumans et al., 2004; Machado et al., 2004; Pires et al., 2004; Thomson et al., 2004; Rodrigues et al., 2005a,b), whereas others were newly determined. New sequences were additionally determined and had their subtype assignment and absence of contamination assured by phylogenetic and bootscanning analyses as described previously (Soares et al., 2007). "
ABSTRACT: The goal of this work was to compare the differences between human immunodeficiency virus type 1 (HIV-1) of B and F1 subtypes in the acquisition of major and minor protease inhibitor (PI)-associated resistance mutations and of other polymorphisms at the protease (PR) gene, through a cross sectional study. PR sequences from subtypes B and F1 isolates matched according to PI exposure time from Brazilian patients were included in this study. Sequences were separated in four groups: 24 and 90 from children and 141 and 99 from adults infected with isolates of subtypes F1 and B, respectively. For comparison, 211 subtype B and 79 subtype F1 PR sequences from drug-naïve individuals were included. Demographic and clinical data were similar among B- and F1-infected patients. In untreated patients, mutations L10V, K20R, and M36I were more frequent in subtype F1, while L63P, A71T, and V77I were more prevalent in subtype B. In treated patients, K20M, D30N, G73S, I84V, and L90M, were more prevalent in subtype B, and K20T and N88S were more prevalent in subtype F1. A higher proportion of subtype F1 than of subtype B strains containing other polymorphisms was observed. V82L mutation was present with increased frequency in isolates from children compared to isolates from adults infected with both subtypes. We could observe a faster resistance emergence in children than in adults, during treatment with protease inhibitors. This data provided evidence that, although rates of overall drug resistance do not differ between subtypes B and F1, the former accumulates resistance at higher proportion in specific amino acid positions of protease when compared to the latter.Infection Genetics and Evolution 11/2008; 9(1):62-70. DOI:10.1016/j.meegid.2008.10.002 · 3.26 Impact Factor
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- "CRFs.html). In Brazil, HIV-1 subtypes B, F and C, as well as unique and circulating recombinant forms, are co-circulating (Bongertz et al., 2000; Csillag, 1994; De Sa Filho et al., 2006; Louwagie et al., 1994; Morgado et al., 1998; Morgado et al., 1994; Potts et al., 1993; Ramos et al., 1999; Sa Filho et al., 2005; Santos et al., 2006; Thomson et al., 2004). In 1993 (Potts et al., 1993), it became apparent that Brazilian subtype B strains contained an antigenically distinct variant that has a signature motif at the tip of the V3 loop, with tryptophan rather than proline at position 328 in the HIV-1 envelope (Casseb et al., 1998; da Costa et al., 1995; Potts et al., 1993). "
ABSTRACT: Half of subtype B Brazilian HIV-1 harbors the V3 tip GWGR instead of the GPGR. To investigate the evolution of GW variants, we analyzed 81 env sequences and 5 full-length GW genomes from antiretroviral-naive individuals sampled between 1983 and 1999. Phylogenetic analysis indicated that GW strains intermingle in the tree with other subtype B sequences. The mean d(N)/d(S) values of GW strains were proximal to those of the other sequences, regardless of sampling years or clinical status. In sequences from patients with CD4+ T cell counts >or=200 cells/microL, the mean d(N)/d(S) ratio was greater than one, suggesting a positive selection. The prevalence of GW variants was lower among individuals in whom disease progressed. This is probably attributable to the fact that tryptophan is replaced by other amino acids over time, whereas the GP motif does not evolve as rapidly.Virology 09/2008; 381(2):184-93. DOI:10.1016/j.virol.2008.08.014 · 3.28 Impact Factor