ArticleJournal of virology2005
CD8 T cells require gamma interferon to clear borna disease virus from the brain and prevent immune system-mediated neuronal damage.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Interferon and TLR genes, but not endogenous bornavirus-like elements, limit BoDV1 replication after intracerebral infection.PLoS pathogens · 2025Article
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- Human Borna disease virus 1 encephalitis shows marked pro-inflammatory biomarker and tissue immunoactivation during the course of disease.Emerging microbes & infections · 2022Article
- Avian Bornavirus Research-A Comprehensive Review.Viruses · 2022Review
- Why does viral RNA sometimes persist after recovery from acute infections?PLoS biology · 2022Article
- Persistent RNA virus infection is short-lived at the single-cell level but leaves transcriptomic footprints.The Journal of experimental medicine · 2021Article
- T cell engagement of cross-presenting microglia protects the brain from a nasal virus infection.Science immunology · 2020Article
- Article
- The neonatal anti-viral response fails to control measles virus spread in neurons despite interferon-gamma expression and a Th1-like cytokine profile.Journal of neuroimmunology · 2018Article
- Assessment of listing and categorisation of animal diseases within the framework of the Animal Health Law (Regulation (EU) No 2016/429): Borna disease.EFSA journal. European Food Safety Authority · 2017Article
- Interferon gamma modulation of disease manifestation and the local antibody response to alphavirus encephalomyelitis.The Journal of general virology · 2016Article
- Interferon gamma protects neonatal neural stem/progenitor cells during measles virus infection of the brain.Journal of neuroinflammation · 2016Article
- IL-1R1 signaling regulates CXCL12-mediated T cell localization and fate within the central nervous system during West Nile Virus encephalitis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- Immune-mediated loss of transgene expression from virally transduced brain cells is irreversible, mediated by IFNγ, perforin, and TNFα, and due to the elimination of transduced cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- The critical role of antigen-presentation-induced cytokine crosstalk in the central nervous system in multiple sclerosis and experimental autoimmune encephalomyelitis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2011Review
- Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis.Brain pathology (Zurich, Switzerland) · 2010Article
- T cells facilitate recovery from Venezuelan equine encephalitis virus-induced encephalomyelitis in the absence of antibody.Journal of virology · 2010Article
- T cells can mediate viral clearance from ependyma but not from brain parenchyma in a major histocompatibility class I- and perforin-independent manner.Brain : a journal of neurology · 2010Article
- Interferon-gamma prevents death of bystander neurons during CD8 T cell responses in the brain.The American journal of pathology · 2009Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Borna disease virus (BDV) frequently causes meningoencephalitis and fatal neurological disease in young but not old mice of strain MRL. Disease does not result from the virus-induced destruction of infected neurons. Rather, it is mediated by H-2(k)-restricted antiviral CD8 T cells that recognize a peptide derived from the BDV nucleoprotein N. Persistent BDV infection in mice is not spontaneously cleared. We report here that N-specific vaccination can protect wild-type MRL mice but not mutant MRL mice lacking gamma interferon (IFN-gamma) from persistent infection with BDV. Furthermore, we observed a significant degree of resistance of old MRL mice to persistent BDV infection that depended on the presence of CD8 T cells. We found that virus initially infected hippocampal neurons around 2 weeks after intracerebral infection but was eventually cleared in most wild-type MRL mice. Unexpectedly, young as well as old IFN-gamma-deficient MRL mice were completely susceptible to infection with BDV. Moreover, neurons in the CA1 region of the hippocampus were severely damaged in most diseased IFN-gamma-deficient mice but not in wild-type mice. Furthermore, large numbers of eosinophils were present in the inflamed brains of IFN-gamma-deficient mice but not in those of wild-type mice, presumably because of increased intracerebral synthesis of interleukin-13 and the chemokines CCL1 and CCL11, which can attract eosinophils. These results demonstrate that IFN-gamma plays a central role in host resistance against infection of the central nervous system with BDV and in clearance of BDV from neurons. They further indicate that IFN-gamma may function as a neuroprotective factor that can limit the loss of neurons in the course of antiviral immune responses in the brain.
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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.