Interferon and TLR genes, but not endogenous bornavirus-like elements, limit BoDV1 replication after intracerebral infection

Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes...

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Published inPLoS pathogens Vol. 21; no. 5; p. e1013165
Main Authors Koide, Rie, Abe, Takaya, Harimoto, Taichi, Kamada, Anselmo Jiro, Saito, Yuka, Guerrini, Matteo, Fujii, Asami, Parrish, Erica, Horie, Masayuki, Kiyonari, Hiroshi, Yamamoto, Kazuhiko, Tomonaga, Keizo, Parrish, Nicholas F
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 09.05.2025
Public Library of Science (PLoS)
Subjects
Analysis
Animals
Antiviral agents
Biology and Life Sciences
Borna Disease - genetics
Borna Disease - immunology
Borna Disease - virology
Borna disease virus - genetics
Borna disease virus - immunology
Borna disease virus - physiology
Brain - immunology
Brain - virology
Control
Dosage and administration
Engineering and Technology
Genetic aspects
Identification and classification
Immunity, Innate
Interferon
Interferon-gamma - genetics
Interferon-gamma - immunology
Medicine and Health Sciences
Membrane Glycoproteins - genetics
Membrane Glycoproteins - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Research and Analysis Methods
RNA viruses
RNA, Small Interfering - genetics
RNA, Small Interfering - immunology
Toll-Like Receptor 7 - genetics
Toll-Like Receptor 7 - immunology
Toll-like receptors
Virus Replication - genetics
Virus Replication - immunology
Japan
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Abstract Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wild-type under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates.
AbstractList Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wild-type under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates.
Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wildtype under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates.Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wildtype under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates.
Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wild-type under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates. The study examined the immune response to Borna disease virus 1 (BoDV1), which infects both animals and humans. Previous studies suggest that endogenous bornavirus-like nucleoprotein elements (EBLNs) within mammalian genomes might contribute to antiviral immunity against BoDV1 through a novel mechanism involving piRNA silencing. To dissect the potential role of EBLNs in BoDV1 immunity at a genetic level, we engineered EBLN knockout (KO) mice lacking all three piRNA-producing EBLNs. These mice, along with other KO mice lacking specific immune factors, were injected intracerebrally with BoDV1. The study confirmed that conventional immune pathways involving interferon gamma and Toll-like receptor 7 (TLR7) are more critical for controlling BoDV1 infection compared to the proposed mechanism involving EBLN-derived piRNAs, at least in the context of brain infections in newborn mice. These findings suggest that, while EBLNs might play a role in different scenarios, conventional immune pathways are likely the primary defense against BoDV1 infection, particularly in newborn mouse brains. Further research is needed to determine the significance of EBLNs in antiviral immunity.
Audience Academic
Author Koide, Rie
Parrish, Nicholas F
Abe, Takaya
Harimoto, Taichi
Kamada, Anselmo Jiro
Tomonaga, Keizo
Yamamoto, Kazuhiko
Guerrini, Matteo
Saito, Yuka
Horie, Masayuki
Parrish, Erica
Kiyonari, Hiroshi
Fujii, Asami
AuthorAffiliation 7 Laboratory of RNA Viruses, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan
1 Genome Immunobiology RIKEN Hakubi Research Team, RIKEN Cluster for Pioneering Research and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
8 Laboratory of RNA Viruses, Department of Mammalian Regulatory Network, Graduate School of Biostudies, Kyoto University, Kyoto, Japan
3 Department of Biology, University of Oxford, Oxford, United Kingdom
2 Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan
5 Graduate School of Veterinary Science, Osaka Metropolitan University, Osaka, Japan
The Ohio State University, UNITED STATES OF AMERICA
4 Laboratory for Autoimmune Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan
9 Department of Molecular Virology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
6 Osaka International Research Center for Infe
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The authors have declared that no competing interests exist.
Current address: Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
ORCID 0000-0002-6971-8016
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Snippet Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune...
Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, humans. What constitutes a protective immune...
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StartPage e1013165
SubjectTerms Analysis
Animals
Antiviral agents
Biology and Life Sciences
Borna Disease - genetics
Borna Disease - immunology
Borna Disease - virology
Borna disease virus - genetics
Borna disease virus - immunology
Borna disease virus - physiology
Brain - immunology
Brain - virology
Control
Dosage and administration
Engineering and Technology
Genetic aspects
Identification and classification
Immunity, Innate
Interferon
Interferon-gamma - genetics
Interferon-gamma - immunology
Medicine and Health Sciences
Membrane Glycoproteins - genetics
Membrane Glycoproteins - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Research and Analysis Methods
RNA viruses
RNA, Small Interfering - genetics
RNA, Small Interfering - immunology
Toll-Like Receptor 7 - genetics
Toll-Like Receptor 7 - immunology
Toll-like receptors
Virus Replication - genetics
Virus Replication - immunology
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Title Interferon and TLR genes, but not endogenous bornavirus-like elements, limit BoDV1 replication after intracerebral infection
URI https://www.ncbi.nlm.nih.gov/pubmed/40344162
https://www.proquest.com/docview/3202399084
https://pubmed.ncbi.nlm.nih.gov/PMC12112416
https://doaj.org/article/ffc9ff88ae2d431fa879e8e365d1a85a
Volume 21
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