Infectious pancreatic necrosis virus triggers antiviral immune response in rainbow trout red blood cells, despite not being infective

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Abstract

Background: Some fish viruses, such as piscine orthoreovirus and infectious salmon anemia virus, target red blood cells (RBCs), replicate inside them and induce an immune response. However, the roles of RBCs in the context of infectious pancreatic necrosis virus (IPNV) infection have not been studied yet.

Methods: Ex vivo rainbow trout RBCs were obtained from peripheral blood, Ficoll purified and exposed to IPNV in order to analyze infectivity and immune response using RT-qPCR, immune fluorescence imaging, flow cytometry and western-blotting techniques.

Results: IPNV could not infect RBCs; however, IPNV increased the expression of the INF1-related genes ifn-1, pkr and mx genes. Moreover, conditioned media from IPNV-exposed RBCs conferred protection against IPNV infection in CHSE-214 fish cell line.

Conclusions: Despite not being infected, rainbow trout RBCs could respond to IPNV with increased expression of antiviral genes. Fish RBCs could be considered as mediators of the antiviral response and therefore targets of new strategies against fish viral infections. Further research is ongoing to completely understand the molecular mechanism that triggers this antiviral response in rainbow trout RBCs.

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Most cited references 47

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Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method.

Kenneth Livak, Thomas D. Schmittgen (2001)

The two most commonly used methods to analyze data from real-time, quantitative PCR experiments are absolute quantification and relative quantification. Absolute quantification determines the input copy number, usually by relating the PCR signal to a standard curve. Relative quantification relates the PCR signal of the target transcript in a treatment group to that of another sample such as an untreated control. The 2(-Delta Delta C(T)) method is a convenient way to analyze the relative changes in gene expression from real-time quantitative PCR experiments. The purpose of this report is to present the derivation, assumptions, and applications of the 2(-Delta Delta C(T)) method. In addition, we present the derivation and applications of two variations of the 2(-Delta Delta C(T)) method that may be useful in the analysis of real-time, quantitative PCR data. Copyright 2001 Elsevier Science (USA).

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Interferon-stimulated genes and their antiviral effector functions

John W Schoggins, Charles Rice (2011)

Highlights ► IFN induces a diverse range of antiviral effectors. ► Each virus has a unique, but partially overlapping, antiviral ‘ISG profile’. ► IFN effectors target multiple stages in the virus life cycle. ► The IFN signaling pathway is highly self-reinforcing. ► Viruses may hijack IFN effectors to promote replication.

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Type I interferon inhibits interleukin-1 production and inflammasome activation.

Greta Guarda, Marion Braun, Francesco Staehli … (2011)

Type I interferon (IFN) is a common therapy for autoimmune and inflammatory disorders, yet the mechanisms of action are largely unknown. Here we showed that type I IFN inhibited interleukin-1 (IL-1) production through two distinct mechanisms. Type I IFN signaling, via the STAT1 transcription factor, repressed the activity of the NLRP1 and NLRP3 inflammasomes, thereby suppressing caspase-1-dependent IL-1β maturation. In addition, type I IFN induced IL-10 in a STAT1-dependent manner; autocrine IL-10 then signaled via STAT3 to reduce the abundance of pro-IL-1α and pro-IL-1β. In vivo, poly(I:C)-induced type I IFN diminished IL-1β production in response to alum and Candida albicans, thus increasing susceptibility to this fungal pathogen. Importantly, monocytes from multiple sclerosis patients undergoing IFN-β treatment produced substantially less IL-1β than monocytes derived from healthy donors. Our findings may thus explain the effectiveness of type I IFN in the treatment of inflammatory diseases but also the observed "weakening" of the immune system after viral infection. Copyright © 2011 Elsevier Inc. All rights reserved.

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Author and article information

Contributors

Ivan Nombela: Role: Formal AnalysisRole: InvestigationRole: MethodologyRole: ValidationRole: VisualizationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing

ORCID: https://orcid.org/0000-0001-8436-2081

Aurora Carrion: Role: Formal AnalysisRole: Investigation

Sara Puente-Marin: Role: Investigation

Verónica Chico: Role: Formal AnalysisRole: InvestigationRole: Writing – Review & Editing

Luis Mercado: Role: Resources

Luis Perez: Role: Writing – Review & Editing

ORCID: https://orcid.org/0000-0003-4078-8763

Julio Coll: Role: Writing – Review & Editing

Maria del Mar Ortega-Villaizan: Role: ConceptualizationRole: Formal AnalysisRole: Funding AcquisitionRole: InvestigationRole: MethodologyRole: Project AdministrationRole: ResourcesRole: SupervisionRole: ValidationRole: VisualizationRole: Writing – Original Draft PreparationRole: Writing – Review & Editing

ORCID: https://orcid.org/0000-0003-2065-0601

Journal

Journal ID (nlm-ta): F1000Res

Journal ID (iso-abbrev): F1000Res

Journal ID (pmc): F1000Research

Title: F1000Research

Publisher: F1000 Research Limited (London, UK )

ISSN (Electronic): 2046-1402

Publication date (Electronic): 13 December 2017

Publication date Collection: 2017

Volume: 6

Electronic Location Identifier: 1968

Affiliations

[1 ]Instituto de Biología Molecular y Celular, Miguel Hernández University, Elche, Spain

[2 ]Institute of Biology, Catholic Pontifical University of Valparaiso, Valparaiso, Chile

[3 ]Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Madrid, Spain

[1 ]Department of Food Safety and Infection Biology, Norwegian University of Life Sciences, Oslo, Norway

[2 ]Norwegian Veterinary Institute, Oslo, Norway

[1 ]Department of Biology, University of Waterloo, Waterloo, ON, Canada

Universidad Miguel Hernandez, Spain

[1 ]Department of Food Safety and Infection Biology, Norwegian University of Life Sciences, Oslo, Norway

[2 ]Norwegian Veterinary Institute, Oslo, Norway

Universidad Miguel Hernandez, Spain

Author notes

[a ] mortega-villaizan@ 123456umh.es

No competing interests were disclosed.

Competing interests: No competing interests were disclosed.

Author information

Ivan Nombela https://orcid.org/0000-0001-8436-2081

Luis Perez https://orcid.org/0000-0003-4078-8763

Maria del Mar Ortega-Villaizan https://orcid.org/0000-0003-2065-0601

Article

DOI: 10.12688/f1000research.12994.2

PMC ID: 5747336

PubMed ID: 29333244

SO-VID: 033c9865-7221-464d-9299-d35f78d4ce11

License:

This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date accepted : 22 December 2017

Funding

Funded by: European Research Council

Award ID: GA639249

This work was supported by the European Research Council (ERC starting grant 2014 GA639249).

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Infectious pancreatic necrosis virus triggers antiviral immune response in rainbow trout red blood cells, despite not being infective

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Most cited references 47

Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method.

Interferon-stimulated genes and their antiviral effector functions

Type I interferon inhibits interleukin-1 production and inflammasome activation.

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