Susceptibility of rat immortalized neuronal cell line Rn33B expressing equine major histocompatibility class 1 to equine herpesvirus-1 infection is differentiation dependent.
Animals
Cell Differentiation
Cell Line
Encephalomyelitis
/ veterinary
Herpesviridae Infections
Herpesvirus 1, Equid
/ pathogenicity
Histocompatibility Antigens Class I
/ metabolism
Horse Diseases
/ virology
Horses
Immediate-Early Proteins
/ metabolism
Interferons
/ metabolism
Mice
Neurons
/ metabolism
Rats
Virus Internalization
Rn33B
equine herpesvirus-1
horses
nervous system diseases
neuron
Journal
Microbiology and immunology
ISSN: 1348-0421
Titre abrégé: Microbiol Immunol
Pays: Australia
ID NLM: 7703966
Informations de publication
Date de publication:
Feb 2020
Feb 2020
Historique:
received:
28
08
2019
revised:
31
10
2019
accepted:
11
11
2019
pubmed:
24
11
2019
medline:
15
5
2020
entrez:
24
11
2019
Statut:
ppublish
Résumé
Equine herpesvirus-1 (EHV-1), which causes encephalomyelitis in horses, shows endotheliotropism in the central nervous system of horses, and generally does not infect neurons. However, little is known about the mechanism underlying the resistance of neuron to EHV-1, due to the lack of convenient cell culture systems. In this study, we examined EHV-1 infection in immortalized Rn33B rat neuronal cells, which differentiate into neurons when cultured under nonpermissive conditions. Because murine cell lines are resistant to EHV-1 infections due to the lack of functional entry receptors for EHV-1, we used an Rn33B-derived cell line that stably expresses the equine MHC class 1 molecule, which acts as EHV-1 entry receptor (Rn33B-A68B2M cells). EHV-1 infected undifferentiated Rn33B-A68B2M cells more efficiently than differentiated cells, resulting in the production of progeny virus in the former but not in the latter. By contrast, both differentiated and undifferentiated cells infected with herpes simplex virus-1 produced infectious viral progeny. While EHV-1 infection induced stronger expression of IFN alpha gene in differentiated cells than in undifferentiated cells, downstream IFN responses, including phosphorylation of STAT1 (signal transducer and activator of transcription 1) and expression of IFN-stimulated genes, were not activated regardless of whether cells were differentiated or not. These results suggest that neuronal differentiation of RN33B-A68B2M cells reduced their susceptibility to EHV-1, which is not due to different IFN responses. This culture system may be useful as an in vitro model for studying neuron-specific resistance to EHV-1, by investigating viral and host factors responsible for the difference in susceptibility between differentiated and undifferentiated cells.
Identifiants
pubmed: 31758567
doi: 10.1111/1348-0421.12761
doi:
Substances chimiques
Histocompatibility Antigens Class I
0
Immediate-Early Proteins
0
Interferons
9008-11-1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
123-132Subventions
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : Grant-in-Aid for Scientific Research (B)/16H05022
Informations de copyright
© 2019 The Societies and John Wiley & Sons Australia, Ltd.
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