West Nile Virus Infections in (European) Birds

¹Department of Viroscience, Erasmus Medical Centre, Rotterdam, The Netherlands

²Artemis One Health Research Institute, Utrecht, The Netherlands

³Department of Molecular Medicine, University of Padova, Padova, Italy

Corresponding Author:

Penelope Koraka
Department of Virology, Viroscience Laboratory
Erasmus Medical Centre, 3015CN, Rotterdam, The Netherlands
Tel: +3110-7044279
Fax: +3110-7044760
E-mail: p.koraka@erasmusmc.nl

Received date: August 14, 2016; Accepted date: April 19, 2016; Published date: April 22, 2016

Citation: Koraka P, Barzon L, Martina BEE (2016) West Nile Virus Infections in (European) Birds . J Neuroinfect Dis 7:226. doi:10.4172/2314-7326.1000226

Copyright: © 2016 Koraka P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Neuroinfectious Diseases

Commentary

West Nile virus (WNV), a member of the Flaviviridae family is an important emerging pathogen transmitted by mosquitoes of the Culex sp . wild-and (peri) domesticated birds act as the natural hosts of WNV. Birds are not only susceptible to WNV, but also participate in maintaining the transmission cycle. WNV emerged in North America in 1999 and its emergence was associated with high numbers of neuroinvasive disease in humans and horses. In general, WNV outbreaks were preceded by mass mortality in birds, especially birds belonging to the family Corvidae proved to be particularly susceptible [1]. Today, crows serve as an important early warning system in the USA to monitor WNV activity [2]. WNV outbreaks have been reported in Europe since 1950s. These outbreaks were small and remained focal. In contrast to the USA, bird mortality has not been reported in Europe. The emergence of a lineage 2 WNV coincided with increased reports of neuroinvasive disease in Europe. The WNV strains that have been characterized in Europe are very heterogeneous (Figure 1). This heterogeneity of WNV, at lineage level, together with the appearance of point mutations potentially affecting virulence and/or transmissibility, and the co-circulation of other flaviviruses infecting birds and humans, have important consequences for understanding their ecology and pathogenicity.

Figure 1: Phylogenetic tree of (European) WNV isolates depicting the different lineages of WNV as well as the phylogenetic differences of virulent and avirulent European strains.

A couple of hypotheses have been proposed and investigated to explain these observations: (1) European birds are not susceptible to natural WNV infection, (2) WNV strains in Europe are less virulent compared to the American viruses, (3) Culex mosquitoes in Europe are not competent to transmit WNV to birds, (4) The feeding behavior of WNV infected Culex mosquitoes is different. These hypotheses have been addressed by our laboratory and others providing valuable answers, which allows for more tailored surveillance programs. Specifically, it has been shown that carrion crows are susceptible to experimental infection with certain WNV strains and therefore carrion crows could act as potential amplifying hosts in Europe [3,4]. In our laboratory, we have also shown that jackdaws can be productively infected and succumb to WNV infection. Although approximately 50% of this bird species is susceptible to lethal infection, jackdaws could function as sentinel to follow WNV activity in Europe [5]. Nevertheless, these experiments clearly showed that not all WNV strains that circulate in Europe can cause lethal infection in these birds [4,5]. Characterization of European WNV strains in mice has revealed little differences in virulence between the different strains [6]. However, clear differences in virulence were reported in birds, which do not correlate with virulence in mice and humans. Due to these differences in virulence, we propose a surveillance system in birds, which is based on identifying antibodies to WNV, and when possible the genotype, since active surveillance may only reveal circulation of WNV strains that are virulent to birds.

Mosquitoes from the Culex biotype pipiens pipiens are competent to transmit WNV in Europe and once infected by WNV their feeding behavior for birds do not change [7]. For an arthropod-borne virus like WNV, vector competence is strongly linked to transmissibility of the virus. Surprisingly, it was shown that European mosquitoes are somewhat better in transmitting WNV, making these Culex species competent vectors for WNV. Therefore, lack of bird mortality in Europe cannot be explained by any of the hypotheses mentioned above. An alternative explanation to the lack of bird mortality in Europe is that bird mortality is so low and does not exceed the threshold of detection with current surveillance programs.

To date there is no specific treatment of WNV neuroinvasive disease. Our limited knowledge of the pathogenesis at the cellular and molecular level still hampers the development of intervention strategies to reduce mortality and long-term functional deficits in survivors of WNV encephalitis. Understanding the correlates of virulence and pathogenesis of WNV neuroinvasive disease using stateof- the art technology could allow the identification of biomarkers and leads for novel treatment protocols. We have used the mouse model to study determinants of virulence [6,8] and to identify potential biomarkers [9]. Some of these markers have been validated using samples of human clinical cases [10]. At least two potential biomarkers were identified. Further studies are needed to elucidate the importance of these biomarkers for diagnostics or therapeutic purposes.

Taken together, it is clear that European birds are as susceptible to WNV infection as their North American counterparts. Therefore, intrinsic resistance of European birds cannot explain why mass mortality among birds has not been reported in Europe. Since WNV specific antibodies were not detected in any of the collected birds, the hypothesis of herd immunity is unlikely and therefore not sufficient to explain lack of bird mortality in Europe during WNV outbreaks. Avirulent strains circulates in Europe, but their low-frequency cannot explain the lack of mass mortality amongst birds. In addition, no other species have been reported to act as reservoir species for WNV transmission. It is therefore important to continue our efforts to understand the factors that drive ecology, transmission and pathogenesis of WNV disease.

Acknowledgements

The research leading to several of the results presented here, has received complete funding from the European community's seventh framework programme (FP7/2007-2013) under the project "VECTORIE", EC grant agreement number 261466. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. B.E.E. Martina was the coordinator and Koraka was among the principle investigators of VECTORIE.

References

1. Wheeler SS, Barker CM, Fang Y, Armijos MV, Carroll BD, et al. (2009) Differential Impact of West Nile Virus on California Birds. Condor 111: 1-20.
2. Eidson M, Schmit K, Hagiwara Y, Anand M, Backenson PB, et al. (2005) Dead crow density and West Nile virus monitoring, New York. Emerg Infect Dis 11: 1370-1375.
3. Dridi M, Vangeluwe D, Lecollinet S, van den Berg T, Lambrecht B (2013) Experimental infection of Carrion crows (Corvus corone) with two European West Nile virus (WNV) strains. Vet Microbiol 165: 160-166.
4. Lim SM, Brault AC, Amerongen GV, Bosco-Lauth AG, Romo H, et al. (2015) Susceptibility of Carrion Crows to Experimental Infection with Lineage 1 and 2 West Nile Viruses. Emerg Infect Dis 21: 1357-1365.
5. Lim SM, Brault AC, van Amerongen G, Sewbalaksing VD, Osterhaus AD, et al. (2014) Susceptibility of European jackdaws (Corvus monedula) to experimental infection with lineage 1 and 2 West Nile viruses. J Gen Virol 95: 1320-1329.
6. Lim SM, Koraka P, van Boheemen S, Roose JM, Jaarsma D, et al. (2013) Characterization of the mouse neuroinvasiveness of selected European strains of West Nile virus. PLoS One 8: e74575.
7. Fros JJ, Geertsema C, Vogels CB, Roosjen PP, Failloux AB, et al. (2015) West Nile Virus: High Transmission Rate in North-Western European Mosquitoes Indicates Its Epidemic Potential and Warrants Increased Surveillance. PLoS Negl Trop Dis 9: e0003956.
8. Szentpáli-Gavallér K, Lim SM, Dencs�? L, Bányai K, Koraka P, et al. (2016) In Vitro and in Vivo Evaluation of Mutations in the NS Region of Lineage 2 West Nile Virus Associated with Neuroinvasiveness in a Mammalian Model. Viruses 8.
9. Fraisier C, Camoin L, Lim SM, Bakli M, Belghazi M, et al. (2013) Altered protein networks and cellular pathways in severe west nile disease in mice. PLoS One 8: p. e68318.
10. Fraisier C, Papa A, Granjeaud S, Hintzen R, Martina B, et al. (2014) Cerebrospinal fluid biomarker candidates associated with human WNV neuroinvasive disease. PLoS One 9: e93637.