<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Nguyen Giang Thu</style></author><author><style face="normal" font="default" size="100%">Fabienne Rauw</style></author><author><style face="normal" font="default" size="100%">Mieke Steensels</style></author><author><style face="normal" font="default" size="100%">Ingrao, Fiona</style></author><author><style face="normal" font="default" size="100%">Bonfante, Francesco</style></author><author><style face="normal" font="default" size="100%">Irit Davidson</style></author><author><style face="normal" font="default" size="100%">Bénédicte Lambrecht</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Study of the underlying mechanisms and consequences of pathogenicity differences between two in vitro selected G1-H9N2 clones originating from a single isolate.</style></title><secondary-title><style face="normal" font="default" size="100%">Vet Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Chickens</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemagglutination Inhibition Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunity, Innate</style></keyword><keyword><style  face="normal" font="default" size="100%">In Vitro Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza A Virus, H9N2 Subtype</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza in Birds</style></keyword><keyword><style  face="normal" font="default" size="100%">Poultry Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Plaque Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">virulence</style></keyword><keyword><style  face="normal" font="default" size="100%">Virus Shedding</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Mar 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">50</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The G1-H9N2 avian influenza virus (AIV) has caused significant economic losses in the commercial poultry industry due to reduced egg production and increased mortality. The field observations have shown that H9N2 viruses circulate and naturally mix with other pathogens and these simultaneous infections can exacerbate disease. To avoid an incorrect virus characterization, due to co-infection, isolates were purified by in vitro plaque assays. Two plaque purified G1-H9N2 clones, selected on different cell types, named MDCK-and CEF-clone in regards to the cell culture used, were studied in vivo, revealing two different virulence phenotypes. Subsequently, the underlying mechanisms were studied. Specifically, the phenotypical outcome of SPF bird infection by the two clones resulted in completely different clinical outcomes. These differences in clinical outcome were used to study the factors behind this output in more detail. Further studies demonstrated that the more severe disease outcome associated with the MDCK-clone involves a strong induction of pro-inflammatory cytokines and a lack of type I interferon production, whereas the mild disease outcome associated with the CEF-clone is related to a greater antiviral cytokine response. The immunosuppressive effect of the MDCK-clone on splenocytes was further demonstrated via ChIFN-γ lack production after ex vivo mitogenic stimulation. Genome sequencing of the two clones identified only four amino acid differences including three in the HA sequence (HA-E198A, HA-R234L, HA-E502D-H9 numbering) and one in the NA sequence (NA-V33M). In the present study, valuable insights on the mechanisms responsible for AI pathogenicity and molecular mechanisms of H9N2 infections in chicken were obtained while highlighting the impact of the cells viruses are grown on their virulence.&lt;/p&gt;
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