ArticlePLoS pathogens2012
Gammaherpesvirus latency accentuates EAE pathogenesis: relevance to Epstein-Barr virus and multiple sclerosis.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Repurposing Licensed Drugs with Activity Against Epstein-Barr Virus for Treatment of Multiple Sclerosis: A Systematic Approach.CNS drugs · 2025Pooled it
- Why Is MS a More Frequent Complication of EBV Infection in Females?Immunological reviews · 2026Review
- 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
- Memory inflation: Beyond the acute phase of viral infection.Cell proliferation · 2024Review
- The EBV-MS connection: the enigma remains.Frontiers in immunology · 2024Article
- 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
- Editorial: Environmental factors influencing the immune functions during multiple sclerosis.Frontiers in immunology · 2023Article
- Expression of the human herpesvirus 6A latency-associated transcript U94A impairs cytoskeletal functions in human neural cells.Molecular and cellular neurosciences · 2022Article
- Gammaherpesvirus infection drives age-associated B cells toward pathogenicity in EAE and MS.Science advances · 2022Article
- Molecular Mimicry Analyses Unveiled the Human Herpes Simplex and Poxvirus Epitopes as Possible Candidates to Incite Autoimmunity.Pathogens (Basel, Switzerland) · 2022Article
- B cells going viral in the CNS: Dynamics, complexities, and functions of B cells responding to viral encephalitis.Immunological reviews · 2022Review
- Age-associated B cells in autoimmune diseases.Cellular and molecular life sciences : CMLS · 2022Review
- What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?Frontiers in immunology · 2022Review
- Influence of Type I Interferons in Gammaherpesvirus-68 and Its Influence on EAE Enhancement.Frontiers in immunology · 2022Article
- When a virus lies in wait.eLife · 2021Article
- Latent gammaherpesvirus exacerbates arthritis through modification of age-associated B cells.eLife · 2021Article
- Asymptomatic Herpes Simplex Virus Type 1 Infection Causes an Earlier Onset and More Severe Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2021Article
- From Superantigens to "Real" Viral Antigens.Viral immunology · 2020Article
- Epstein-Barr Virus in Multiple Sclerosis: Theory and Emerging Immunotherapies.Trends in molecular medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) has been identified as a putative environmental trigger of multiple sclerosis (MS), yet EBV's role in MS remains elusive. We utilized murine gamma herpesvirus 68 (γHV-68), the murine homolog to EBV, to examine how infection by a virus like EBV could enhance CNS autoimmunity. Mice latently infected with γHV-68 developed more severe EAE including heightened paralysis and mortality. Similar to MS, γHV-68EAE mice developed lesions composed of CD4 and CD8 T cells, macrophages and loss of myelin in the brain and spinal cord. Further, T cells from the CNS of γHV-68 EAE mice were primarily Th1, producing heightened levels of IFN-γ and T-bet accompanied by IL-17 suppression, whereas a Th17 response was observed in uninfected EAE mice. Clearly, γHV-68 latency polarizes the adaptive immune response, directs a heightened CNS pathology following EAE induction reminiscent of human MS and portrays a novel mechanism by which EBV likely influences MS and other autoimmune diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.