ABSTRACT
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.
Subject(s)
Disease Outbreaks/prevention & control , Epidemiological Monitoring , Genomics/methods , Yellow Fever/prevention & control , Yellow Fever/transmission , Yellow fever virus/isolation & purification , Aedes/virology , Age Factors , Animals , Brazil/epidemiology , Disease Outbreaks/statistics & numerical data , Evolution, Molecular , Humans , Phylogeny , Polymerase Chain Reaction , Risk , Sex Factors , Spatio-Temporal Analysis , Yellow Fever/epidemiology , Yellow Fever/virology , Yellow fever virus/classification , Yellow fever virus/geneticsABSTRACT
Heart failure (HF) is a very common condition that, despite advances in treatment, carries significant morbidity and mortality. Although there is good evidence for the treatment of HF with reduced ejection fraction (HFrEF), the treatment for HF with preserved ejection fraction (HFpEF) is not well defined. The renin-angiotensin-aldosterone system (RAAS) has been shown to be an effective target in the treatment of HFrEF using angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone blockade, although the evidence in HFpEF is less clear. This review aims to look first at the evidence for these drugs, and second at the newer drugs that act on the RAAS, namely, direct renin inhibitors, neutral endopeptidase inhibitors, vasopeptidase inhibitors, and angiotensin receptor blockers.