title: Interferon interplay helps tissue cells to cope with SARS-coronavirus infection.
abstract: SARS coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome, is a versatile pathogen armed with a host of factors countering the antiviral type I interferon (IFN) system. Hence, tissue cells infected with SARS-CoV are unable to launch an IFN response. Plasmacytoid dendritic cells, however, produce high levels of IFN after infection. We recently demonstrated that minute amounts of IFN applied before infection (IFN priming) can ameliorate the IFN response of tissue cells to SARS-CoV. IFN priming of SARS-CoV-infected cells activated genes for IFN transcription, IFN signaling, antiviral effector proteins, ubiquitinylation and ISGylation, antigen presentation, and other cytokines and chemokines, whereas IFN treatment or infection alone had no major effect. Thus, the IFN which is produced by plasmacytoid dendritic cells could enable tissue cells to at least partially overturn the SARS-CoV-induced block in innate immune activation.
authors.affiliation: Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Freiburg, Germany.
authors.forename: Thomas
authors.initials: T
authors.lastname: Kuri
authors.forename: Friedemann
authors.initials: F
authors.lastname: Weber
mesh_terms: D000818:Animals; D002460:Cell Line; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D050838:Interferon Regulatory Factor-3 / Q000378:metabolism; D050839:Interferon Regulatory Factor-7 / Q000378:metabolism; D007370:Interferon Type I / Q000096:biosynthesis* / Q000276:immunology* / Q000494:pharmacology; D045473:Severe acute respiratory syndrome-related coronavirus / Q000276:immunology / Q000472:pathogenicity*; D045169:Severe Acute Respiratory Syndrome / Q000276:immunology* / Q000821:virology
chemical_list: D050838:Interferon Regulatory Factor-3; D050839:Interferon Regulatory Factor-7; D007370:Interferon Type I