title: Differential response of the Senegalese sole (Solea senegalensis) Mx promoter to viral infections in two salmonid cell lines.
abstract: Mx proteins are main effectors of the antiviral innate immune defence mediated by type I interferon (IFN I). The IFN I response is under a complex regulation; hence, one of the key issues in understanding virus-host interaction is the knowledge of the regulatory mechanisms governing this response. With this purpose, in this study Chinook salmon embryo cells (CHSE-214) and rainbow trout gonad cells (RTG-2) were transiently transfected with a vector containing the luciferase reporter gene under the control of the Senegalese sole Mx promoter. These transfected cells were infected with infectious pancreatic necrosis virus (IPNV), viral haemorrhagic septicaemia virus (VHSV) and epizootic haematopoietic necrosis virus (EHNV) at different doses in order to study the luciferase fold induction in response to viral infections. Transfected CHSE-214 cells infected with EHNV showed significant induction of the luciferase reporter gene, compared to control non-infected cells, at different times post infection (p.i.). The maximum expression was recorded at 24h p.i. in cells inoculated with 5 × 10(2)TCID50/mL (2.17 folds compared to control cells). In these cells, the infection with IPNV and VHSV did not result in the luciferase expression at any time and doses tested. In transfected RTG-2 cells, VHSV stimulated luciferase expression, obtaining a maximum activity at 48 h p.i. in cells infected with 5 × 10(2)TCID50/mL (2.9 folds compared to control cells), whereas RTG-2 cells infected with IPNV and EHNV did not show significant luciferase activity at any time point. The different induction of the Senegalese sole Mx promoter in CHSE-214 and RTG-2 cells after infection with the same viruses indicates that cell-specific factors are significantly involved in the IFN-signalling response, and, probably, on the success of the strategies of these viruses to escape the IFN mechanisms. The use of these two different cellular systems might be an interesting approach to identify such cellular factors.
authors.affiliation: Universidad de Málaga, Departamento de Genética, Facultad de Ciencias, 29071 Málaga, Spain; Universidad de Málaga, Departamento de Microbiología, Facultad de Ciencias, 29071 Málaga, Spain.
authors.forename: Daniel
authors.initials: D
authors.lastname: Alvarez-Torres
authors.affiliation: Universidad de Málaga, Departamento de Microbiología, Facultad de Ciencias, 29071 Málaga, Spain.
authors.forename: M Carmen
authors.initials: MC
authors.lastname: Alonso
authors.affiliation: Universidad de Málaga, Departamento de Microbiología, Facultad de Ciencias, 29071 Málaga, Spain.
authors.forename: Esther
authors.initials: E
authors.lastname: Garcia-Rosado
authors.affiliation: Marine Scotland, 375 Victoria Road, Aberdeen AB11 9DB, Scotland, United Kingdom.
authors.forename: Bertrand
authors.initials: B
authors.lastname: Collet
authors.affiliation: Universidad de Málaga, Departamento de Genética, Facultad de Ciencias, 29071 Málaga, Spain. Electronic address: bejar@uma.es.
authors.forename: Julia
authors.initials: J
authors.lastname: Béjar
mesh_terms: D000818:Animals; D002460:Cell Line; D005412:Flatfishes / Q000378:metabolism*; D005786:Gene Expression Regulation; D018164:Hemorrhagic Disease Virus, Epizootic / Q000502:physiology; D018061:Infectious pancreatic necrosis virus / Q000502:physiology; D064547:Myxovirus Resistance Proteins / Q000235:genetics / Q000378:metabolism*; D029141:Novirhabdovirus / Q000502:physiology; D017686:Oncorhynchus mykiss; D011401:Promoter Regions, Genetic; D012474:Salmon / Q000196:embryology; D014162:Transfection
chemical_list: D064547:Myxovirus Resistance Proteins