RESUMEN
The yellow fever virus (YFV) epidemic in Brazil is the largest in decades. The recent discovery of YFV in Brazilian Aedes species mosquitos highlights a need to monitor the risk of reestablishment of urban YFV transmission in the Americas. We use a suite of epidemiological, spatial, and genomic approaches to characterize YFV transmission. We show that the age and sex distribution of human cases is characteristic of sylvatic transmission. Analysis of YFV cases combined with genomes generated locally reveals an early phase of sylvatic YFV transmission and spatial expansion toward previously YFV-free areas, followed by a rise in viral spillover to humans in late 2016. Our results establish a framework for monitoring YFV transmission in real time that will contribute to a global strategy to eliminate future YFV epidemics.
Asunto(s)
Brotes de Enfermedades/prevención & control , Monitoreo Epidemiológico , Genómica/métodos , Fiebre Amarilla/prevención & control , Fiebre Amarilla/transmisión , Virus de la Fiebre Amarilla/aislamiento & purificación , Aedes/virología , Factores de Edad , Animales , Brasil/epidemiología , Brotes de Enfermedades/estadística & datos numéricos , Evolución Molecular , Humanos , Filogenia , Reacción en Cadena de la Polimerasa , Riesgo , Factores Sexuales , Análisis Espacio-Temporal , Fiebre Amarilla/epidemiología , Fiebre Amarilla/virología , Virus de la Fiebre Amarilla/clasificación , Virus de la Fiebre Amarilla/genéticaRESUMEN
Renal sodium reabsorption depends on the activity of the Na+,K+-ATPase α/ß heterodimer. Four α (α1-4) and 3 ß (ß1-3) subunit isoforms have been described. It is accepted that renal tubule cells express α1/ß1 dimers. Aldosterone stimulates Na+,K+-ATPase activity and may modulate α1/ß1 expression. However, some studies suggest the presence of ß3 in the kidney. We hypothesized that the ß3 isoform of the Na+,K+-ATPase is expressed in tubular cells of the distal nephron, and modulated by mineralocorticoids. We found that ß3 is highly expressed in collecting duct of rodents, and that mineralocorticoids decreased the expression of ß3. Thus, we describe a novel molecular mechanism of sodium pump modulation that may contribute to the effects of mineralocorticoids on sodium reabsorption.