Green, T.Speck, P.Geng, L.Raftos, D.Beard, M.Helbig, K.2016-06-012016-06-012015Journal of General Virology, 2015; 96(12):3587-35970022-13171465-2099http://hdl.handle.net/2440/99331Little is known about the response of non-model invertebrates, such as oysters, to viral infection. The vertebrate innate immune system detects virus-derived nucleic acids to trigger the type I interferon (IFN)-pathway, leading to the transcription of hundreds of IFN-stimulated genes (ISGs) that exert antiviral functions. Invertebrates were thought to lack the IFN-pathway based on the absence of IFN or ISGs encoded in model-invertebrate genomes. However, the oyster genome encodes many ISGs, including the well-described antiviral protein, viperin. In this study, we characterise oyster-viperin and show it localises to caveolin-1 and inhibits Dengue virus replication in a heterologous model. In a second set of experiments, we provide evidence that the hemolymph from poly(I:C)-injected oysters contains a heat-stable, protease-susceptible factor that induces hemocyte transcription of viperin mRNA in conjunction with upregulation of IFN-regulatory factor. Collectively, these results support the concept that oysters have antiviral systems that are homologous to the vertebrate IFN-pathway.en© 2015 The AuthorsHemolymphAnimalsDengue VirusLipidsProteinsAntiviral AgentsVirus ReplicationSignal TransductionGene Expression RegulationAmino Acid SequenceMolecular Sequence DataOstreidaeCaveolin 1Hot TemperatureOyster viperin retains direct antiviral activity and its transcription occurs via a signalling pathway involving a heat-stable haemolymph proteinJournal article003003714210.1099/jgv.0.0003000003695218000152-s2.0-84949585019216772Beard, M. [0000-0002-4106-1016]