Abstract

The structural risk of West Nile Disease results from the usual functioning of the socio-ecological system, which may favour the introduction of the pathogen, its circulation and the occurrence of disease cases. Its geographic variations result from the local interactions between three components: (i) reservoir hosts, (ii) vectors, both characterized by their diversity, abundance and competence, (iii) and the socio-economic context that impacts the exposure of human to infectious bites. We developed a model of bird-borne structural risk of West Nile Virus (WNV) circulation in Europe, and analysed the association between the geographic variations of this risk and the occurrence of WND human cases between 2002 and 2014. A meta-analysis of WNV serosurveys conducted in wild bird populations was performed to elaborate a model of WNV seropositivity in European bird species, considered a proxy for bird exposure to WNV. Several eco-ethological traits of bird species were linked to seropositivity and the statistical model adequately fitted species-specific seropositivity data (area under the ROC curve: 0.85). Combined with species distribution maps, this model allowed deriving geographic variations of the bird-borne structural risk of WNV circulation. The association between this risk, and the occurrence of WND human cases across the European Union was assessed. Geographic risk variations of bird-borne structural risk allowed predicting WND case occurrence in administrative districts of the EU with a sensitivity of 86% (95% CI: 0.79–0.92), and a specificity of 68% (95% CI: 0.66–0.71). Disentangling structural and conjectural health risks is important for public health managers as risk mitigation procedures differ according to risk type. The results obtained show promise for the prevention of WND in Europe. Combined with analyses of vector-borne structural risk, they should allow designing efficient and targeted prevention measures.

Highlights

  • West Nile disease (WND) is caused by the West Nile virus (WNV) (Flavivirus, Flaviviridae)

  • Application of inclusion/exclusion criteria resulted in 18 papers (Table 1) describing studies conducted in 10 countries -9 European countries and Morocco, and providing original data of WNV seroprevalence in wild birds of species weighing

  • The capacity of a local bird population to support WNV circulation is governed by two parameters that operate on distinct levels [18]: the intrinsic receptivity of birds to WNV, that is based on genetic determinants, whereas the exposure of birds to mosquito bites is rather based on eco-ethological determinants

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Summary

Introduction

West Nile disease (WND) is caused by the West Nile virus (WNV) (Flavivirus, Flaviviridae). The transmission cycle involves wild and domestic birds as main hosts and mosquitoes, mainly of the Culex genus, as vectors. Wild birds and West Nile in Europe amplified and lead to human and horse infections. The latter two are considered dead-end hosts [1]. Ten percent of horses infected by WNV present neurological disorders [4,5]. Most of human and/or equine cases were caused by strains belonging to lineage 1a, characterized by a moderate pathogenicity for horses and humans and a limited or no pathogenicity for birds [7]. Since 2000, WNV epidemiological pattern has evolved with an increase of mortality in some bird species, and a higher incidence of animal and human neurological cases. Lineage 2 strains, so far confined to the south of the Sahara, has been first detected in 2004 in Hungary and thereafter in several countries of central and southern Europe [8,9,10,11,12,13]

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