Percorrer por autor "Lemey, Philippe"
A mostrar 1 - 2 de 2
Resultados por página
Opções de ordenação
- Earlier initiation of antiretroviral treatment coincides with an initial control of the HIV-1 sub-subtype F1 outbreak among men-having-sex-with-men in Flanders, BelgiumPublication . Vinken, Lore; Fransen, Katrien; Cuypers, Lize; Alexiev, Ivailo; Balotta, Claudia; Debaisieux, Laurent; Seguin-Devaux, Carole; Ribas, Sergio García; Gomes, Perpétua; Incardona, Francesca; Kaiser, Rolf; Ruelle, Jean; Sayan, Murat; Paraschiv, Simona; Paredes, Roger; Peeters, Martine; Sönnerborg, Anders; Vancutsem, Ellen; Vandamme, Anne-Mieke; Van den Wijngaert, Sigi; Van Ranst, Marc; Verhofstede, Chris; Stadler, Tanja; Lemey, Philippe; Van Laethem, KristelHuman immunodeficiency virus type 1 (HIV-1) non-B subtype infections occurred in Belgium since the 1980s, mainly amongst migrants and heterosexuals, whereas subtype B predominated in men-having-sex-with-men (MSM). In the last decade, the diagnosis of F1 sub-subtype in particular has increased substantially, which prompted us to perform a detailed reconstruction of its epidemiological history. To this purpose, the Belgian AIDS Reference Laboratories collected HIV-1 pol sequences from all sub-subtype F1-infected patients for whom genotypic drug resistance testing was requested as part of routine clinical follow-up. This data was complemented with HIV-1 pol sequences from countries with a high burden of F1 infections or a potential role in the global origin of sub-subtype F1. The molecular epidemiology of the Belgian subtype F1 epidemic was investigated using Bayesian phylogenetic inference and transmission dynamics were characterized based on birth-death models. F1 sequences were retained from 297 patients diagnosed and linked to care in Belgium between 1988 and 2015. Phylogenetic inference indicated that among the 297 Belgian F1 sequences, 191 belonged to a monophyletic group that mainly contained sequences from people likely infected in Belgium (OR 26.67, 95% CI 9.59–74.15), diagnosed in Flanders (OR 7.28, 95% CI 4.23–12.53), diagnosed at a recent stage of infection (OR 7.19, 95% CI 2.88-17.95) or declared to be MSM (OR 34.8, 95% CI 16.0–75.6). Together with a Spanish clade, this Belgian clade was embedded in the genetic diversity of Brazilian subtype F1 strains and most probably emerged after one or only a few migration events from Brazil to the European continent before 2002. The origin of the Belgian outbreak was dated back to 2002 (95% higher posterior density 2000–2004) and birth-death models suggested that its extensive growth had been controlled (Re < 1) by 2012, coinciding with a time period where delay in antiretroviral treatment initiation substantially declined. In conclusion, phylogenetic reconstruction of the Belgian HIV-1 sub-subtype F1 epidemic illustrates the introduction and substantial dissemination of viral strains in a geographically restricted risk group that was most likely controlled by effective treatment as prevention.
- Tracing the impact of public health interventions on HIV-1 transmission in Portugal using molecular epidemiologyPublication . Vasylyeva, Tetyana I.; Plessis, Louis du; Pineda-Peña, Andrea C.; Kühnert, Denise; Lemey, Philippe; Vandamme, Anne-Mieke; Gomes, Perpétua; Camacho, Ricardo J.; Pybus, Oliver G.; Abecasis, Ana B.; Faria, Nuno R.Background Estimation of temporal changes in human immunodeficiency virus (HIV) transmission patterns can help to elucidate the impact of preventive strategies and public health policies. Methods Portuguese HIV-1 subtype B and G pol genetic sequences were appended to global reference data sets to identify country-specific transmission clades. Bayesian birth-death models were used to estimate subtype-specific effective reproductive numbers (Re). Discrete trait analysis (DTA) was used to quantify mixing among transmission groups. Results We identified 5 subtype B Portuguese clades (26–79 sequences) and a large monophyletic subtype G Portuguese clade (236 sequences). We estimated that major shifts in HIV-1 transmission occurred around 1999 (95% Bayesian credible interval [BCI], 1998–2000) and 2000 (95% BCI, 1998–2001) for subtypes B and G, respectively. For subtype B, Re dropped from 1.91 (95% BCI, 1.73–2.09) to 0.62 (95% BCI,.52–.72). For subtype G, Re decreased from 1.49 (95% BCI, 1.39–1.59) to 0.72 (95% BCI, .63–.8). The DTA suggests that people who inject drugs (PWID) and heterosexuals were the source of most (>80%) virus lineage transitions for subtypes G and B, respectively. Conclusions The estimated declines in Re coincide with the introduction of highly active antiretroviral therapy and the scale-up of harm reduction for PWID. Inferred transmission events across transmission groups emphasize the importance of prevention efforts for bridging populations.