ArticleScientific reports2015
Latent virus infection upregulates CD40 expression facilitating enhanced autoimmunity in a model of multiple sclerosis.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Early antiviral treatment following gammaherpesvirus-68 infection of the central nervous system prevents subsequent multiple sclerosis-like disease.Journal of neuroinflammation · 2025Article
- Epstein-Barr virus infection promotes T cell dysregulation in a humanized mouse model of multiple sclerosis.Science advances · 2025Article
- Host Genetic Variation Has a Profound Impact on Immune Responses Mediating Control of Viral Load in Chronic Gammaherpesvirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Advances in immune checkpoint-based immunotherapies for multiple sclerosis: rationale and practice.Cell communication and signaling : CCS · 2023Review
- Gammaherpesvirus infection drives age-associated B cells toward pathogenicity in EAE and MS.Science advances · 2022Article
- Influence of Type I Interferons in Gammaherpesvirus-68 and Its Influence on EAE Enhancement.Frontiers in immunology · 2022Article
- What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?Frontiers in immunology · 2022Review
- Latent gammaherpesvirus exacerbates arthritis through modification of age-associated B cells.eLife · 2021Article
- Myelin-specific T cells in animals with Japanese macaque encephalomyelitis.Annals of clinical and translational neurology · 2021Article
- Asymptomatic Herpes Simplex Virus Type 1 Infection Causes an Earlier Onset and More Severe Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2021Article
- Primary Peripheral Epstein-Barr Virus Infection Can Lead to CNS Infection and Neuroinflammation in a Rabbit Model: Implications for Multiple Sclerosis Pathogenesis.Frontiers in immunology · 2021Article
- Presence of Epstein-Barr virus DNA in cerebrospinal fluid is associated with greater HIV RNA and inflammation.AIDS (London, England) · 2020Article
- Multiple Sclerosis-Like Symptoms in Mice Are Driven by Latent γHerpesvirus-68 Infected B Cells.Frontiers in immunology · 2020Article
- Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms.Viruses · 2019Review
- Herpes Simplex Virus Type 1 Infection of the Central Nervous System: Insights Into Proposed Interrelationships With Neurodegenerative Disorders.Frontiers in cellular neuroscience · 2019Review
- Herpesvirus trigger accelerates neuroinflammation in a nonhuman primate model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Viruses and endogenous retroviruses in multiple sclerosis: From correlation to causation.Acta neurologica Scandinavica · 2017Review
- Association of CD40 Gene Polymorphisms with Susceptibility to Neuromyelitis Optica Spectrum Disorders.Molecular neurobiology · 2017Article
- Fresh Ideas, Foundational Experiments (FIFE): Immunology and Diabetes 2016 FIFE Symposium.Frontiers in endocrinology · 2017Article
- Th40 cells (CD4+CD40+ Tcells) drive a more severe form of Experimental Autoimmune Encephalomyelitis than conventional CD4 T cells.PloS one · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) has been identified as a putative environmental trigger of multiple sclerosis (MS) by multiple groups working worldwide. Previously, we reported that when experimental autoimmune encephalomyelitis (EAE) was induced in mice latently infected with murine γ-herpesvirus 68 (γHV-68), the murine homolog to EBV, a disease more reminiscent of MS developed. Specifically, MS-like lesions developed in the brain that included equal numbers of IFN-γ producing CD4(+) and CD8(+) T cells and demyelination, none of which is observed in MOG induced EAE. Herein, we demonstrate that this enhanced disease was dependent on the γHV-68 latent life cycle and was associated with STAT1 and CD40 upregulation on uninfected dendritic cells. Importantly, we also show that, during viral latency, the frequency of regulatory T cells is reduced via a CD40 dependent mechanism and this contributes towards a strong T helper 1 response that resolves in severe EAE disease pathology. Latent γ-herpesvirus infection established a long-lasting impact that enhances subsequent adaptive autoimmune responses.
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