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{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,4,15]],"date-time":"2023-04-15T04:56:11Z","timestamp":1681534571082},"reference-count":70,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2023,4,13]],"date-time":"2023-04-13T00:00:00Z","timestamp":1681344000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Intramural collaborative research grants on Henipaviruses at the Friedrich-Loeffler-Institut","award":["HR-0045","HR-0046"]},{"name":"Federal Excellence Initiative of Mecklenburg Western Pomerania and European Social Fund","award":["ESF\/14-BM-A55-0002\/16"]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Respiratory tract epithelium infection plays a primary role in Nipah virus (NiV) pathogenesis and transmission. Knowledge about infection dynamics and host responses to NiV infection in respiratory tract epithelia is scarce. Studies in non-differentiated primary respiratory tract cells or cell lines indicate insufficient interferon (IFN) responses. However, studies are lacking in the determination of complex host response patterns in differentiated respiratory tract epithelia for the understanding of NiV replication and spread in swine. Here we characterized infection and spread of NiV in differentiated primary porcine bronchial epithelial cells (PBEC) cultivated at the air\u2013liquid interface (ALI). After the initial infection of only a few apical cells, lateral spread for 12 days with epithelium disruption was observed without releasing substantial amounts of infectious virus from the apical or basal sides. Deep time course proteomics revealed pronounced upregulation of genes related to type I\/II IFN, immunoproteasomal subunits, transporter associated with antigen processing (TAP)-mediated peptide transport, and major histocompatibility complex (MHC) I antigen presentation. Spliceosomal factors were downregulated. We propose a model in which NiV replication in PBEC is slowed by a potent and broad type I\/II IFN host response with conversion from 26S proteasomes to immunoproteasomal antigen processing and improved MHC I presentation for adaptive immunity priming. NiV induced cytopathic effects could reflect the focal release of cell-associated NiV, which may contribute to efficient airborne viral spread between pigs.<\/jats:p>","DOI":"10.3390\/v15040961","type":"journal-article","created":{"date-parts":[[2023,4,14]],"date-time":"2023-04-14T06:28:12Z","timestamp":1681453692000},"page":"961","source":"Crossref","is-referenced-by-count":0,"title":["Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air\u2013Liquid Interface"],"prefix":"10.3390","volume":"15","author":[{"given":"Martin","family":"M\u00fcller","sequence":"first","affiliation":[{"name":"Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany"}]},{"ORCID":"http:\/\/orcid.org\/0000-0002-8707-3442","authenticated-orcid":false,"given":"Kerstin","family":"Fischer","sequence":"additional","affiliation":[{"name":"Institute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany"}]},{"given":"Elisabeth","family":"Woehnke","sequence":"additional","affiliation":[{"name":"Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany"}]},{"ORCID":"http:\/\/orcid.org\/0000-0001-7997-493X","authenticated-orcid":false,"given":"Luca M.","family":"Zaeck","sequence":"additional","affiliation":[{"name":"Institute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany"}]},
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