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This is an open-access article distributed under the terms of the Creative Commons Attribution License.-- et al. ; Studies exploring the ecological interactions between avian influenza viruses (AIV), natural hosts and the environment are scarce. Most work has focused on viral survival and transmission under laboratory conditions and through mathematical modelling. However, more integrated studies performed under field conditions are required to validate these results. In this study, we combined information on bird community, environmental factors and viral epidemiology to assess the contribution of biotic and abiotic factors in the occurrence of low pathogenic AIV in Spanish wetlands. For that purpose, seven locations in five different wetlands were studied during two years (2007-2009), including seven sampling visits by location. In each survey, fresh faeces (n = 4578) of wild birds and water samples were collected for viral detection. Also, the vegetation structure, water physical properties of wetlands, climatic conditions and wild bird community composition were determined. An overall AIV prevalence of 1.7%±0.4 was detected in faecal samples with important fluctuations among seasons and locations. Twenty-six AIV were isolated from the 78 RRT-PCR positive samples and eight different haemagglutinines and five neuraminidases were identified, being the combination H3N8 the most frequent. Variation partitioning procedures identified the combination of space and time variables as the most important pure factor - independently to other factors - explaining the variation in AIV prevalence (36.8%), followed by meteorological factor (21.5%) and wild bird community composition/vegetation structure (21.1%). These results contribute to the understanding of AIV ecological drivers in Spanish ecosystems and provide useful guidelines for AIV risk assessment identifying potential hotspots of AIV activity. ; This work was financially supported by INIA (Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria), project FAU2006-00019-C03-00 and by Department of Environment, Territorial Planning, Agriculture and Fisheries of the Basque Government. P. Acevedo was supported by a Beatriu de Pinós fellowship funded by Comissionat per a Universitats i Recerca del Departament d'Innovació, Universitats i Empresa, of the Generalitat de Catalunya and the COFUND Programme-Marie Curie Actions under 7th Marc Programme of the European Community. ; Peer Reviewed

Abstract Some outbreaks involving highly pathogenic avian influenza viruses (HPAIV) of subtypes H5 and H7 were caused by avian-to-human transmissions. In nature, different influenza A viruses can reassort leading to new viruses with new characteristics. We decided to investigate the impact that the NS-segment of H5 HPAIV would have on viral pathogenicity of a classical avian H7 HPAIV in poultry, a natural host. We focussed this study based on our previous work that demonstrated that single reassortment of the NS-segment from an H5 HPAIV into an H7 HPAIV changes the ability of the virus to replicate in mammalian hosts. Our present data show that two different H7-viruses containing an NS-segment from H5–types (FPV NS GD or FPV NS VN) show an overall highly pathogenic phenotype compared with the wild type H7–virus (FPV), as characterized by higher viral shedding and earlier manifestation of clinical signs. Correlating with the latter, higher amounts of IFN-β mRNA were detected in the blood of NS-reassortant infected birds, 48 h post-infection (pi). Although lymphopenia was detected in chickens from all AIV-infected groups, also 48 h pi those animals challenged with NS-reassortant viruses showed an increase of peripheral monocyte/macrophage-like cells expressing high levels of IL-1β, as determined by flow cytometry. Taken together, these findings highlight the importance of the NS-segment in viral pathogenicity which is directly involved in triggering antiviral and pro-inflammatory cytokines found during HPAIV pathogenesis in chickens. ; This work was supported by the Spanish Government Grants AGL2007-60434/GAN and AGL2010-22229-C03-01 (Ministry of Science and Innovation, MICINN). J.V-A was supported by FPI-MICINN Training Grant BES-2008-00260. This work was also supported in part by grants from the German Research Foundation (DFG grant GRK1384, fellowship to Z.W.) and from the German Ministry for Education and Research funded "FluResearchNet—Molecular Signatures Determining Pathogenicity and Species Transmission of Influenza A Viruses" (BMBF grant 01 KI 07136, to S.P ; Peer Reviewed