Next Article in Journal
Triphenylamine-Merocyanine-Based D1-A1-π-A2/A3-D2 Chromophore System: Synthesis, Optoelectronic, and Theoretical Studies
Next Article in Special Issue
Delayed Astrogliosis Associated with Reduced M1 Microglia Activation in Matrix Metalloproteinase 12 Knockout Mice during Theiler’s Murine Encephalomyelitis
Previous Article in Journal
Rosiglitazone Enhances Browning Adipocytes in Association with MAPK and PI3-K Pathways During the Differentiation of Telomerase-Transformed Mesenchymal Stromal Cells into Adipocytes
Previous Article in Special Issue
Intranasal Borna Disease Virus (BoDV-1) Infection: Insights into Initial Steps and Potential Contagiosity
Open AccessArticle

Interferon-Stimulated Genes—Mediators of the Innate Immune Response during Canine Distemper Virus Infection

Department of Pathology, University of Veterinary Medicine Hannover, 30559 Hannover, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(7), 1620; https://doi.org/10.3390/ijms20071620
Received: 19 February 2019 / Revised: 25 March 2019 / Accepted: 27 March 2019 / Published: 1 April 2019
The demyelinating canine distemper virus (CDV)-leukoencephalitis represents a translational animal model for multiple sclerosis. The present study investigated the expression of type I interferon (IFN-I) pathway members in CDV-induced cerebellar lesions to gain an insight into their role in lesion development. Gene expression of 110 manually selected genes in acute, subacute and chronic lesions was analyzed using pre-existing microarray data. Interferon regulatory factor (IRF) 3, IRF7, signal transducer and activator of transcription (STAT) 1, STAT2, MX protein, protein kinase R (PKR), 2′-5′-oligoadenylate synthetase (OAS) 1 and interferon-stimulated gene (ISG) 15 expression were also evaluated using immunohistochemistry. Cellular origin of STAT1, STAT2, MX and PKR were determined using immunofluorescence. CDV infection caused an increased expression of the antiviral effector proteins MX, PKR, OAS1 and ISG15, which probably contributed to a restricted viral replication, particularly in neurons and oligodendrocytes. This increase might be partly mediated by IRF-dependent pathways due to the lack of changes in IFN-I levels and absence of STAT2 in astrocytes. Nevertheless, activated microglia/macrophages showed a strong expression of STAT1, STAT2 and MX proteins in later stages of the disease, indicating a strong activation of the IFN-I signaling cascade, which might be involved in the aggravation of bystander demyelination. View Full-Text
Keywords: canine distemper virus; demyelination; immunofluorescence; immunohistochemistry; interferon-regulated factor; interferon-stimulated gene 15; microarray analysis; 2′-5′-oligoadenylate synthetase; protein kinase R; type I interferon canine distemper virus; demyelination; immunofluorescence; immunohistochemistry; interferon-regulated factor; interferon-stimulated gene 15; microarray analysis; 2′-5′-oligoadenylate synthetase; protein kinase R; type I interferon
Show Figures

Graphical abstract

MDPI and ACS Style

Klotz, D.; Gerhauser, I. Interferon-Stimulated Genes—Mediators of the Innate Immune Response during Canine Distemper Virus Infection. Int. J. Mol. Sci. 2019, 20, 1620.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop