ArticleJournal of virology2001
CD8(+) T lymphocytes mediate Borna disease virus-induced immunopathology independently of perforin.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Spillover infections by rustrela virus, borna disease virus 1 and tick-borne encephalitis virus revealed by retrospective screening of mammalian encephalitis of unknown origin.BMC veterinary research · 2025Article
- Interferon and TLR genes, but not endogenous bornavirus-like elements, limit BoDV1 replication after intracerebral infection.PLoS pathogens · 2025Article
- Article
- Avian Bornavirus Research-A Comprehensive Review.Viruses · 2022Review
- Immunopathology of Fatal Human Variegated Squirrel Bornavirus 1 Encephalitis, Germany, 2011-2013.Emerging infectious diseases · 2019Article
- Article
- Are anti-ganglioside antibodies associated with proventricular dilatation disease in birds?PeerJ · 2017Article
- Viral vector vaccines expressing nucleoprotein and phosphoprotein genes of avian bornaviruses ameliorate homologous challenge infections in cockatiels and common canaries.Scientific reports · 2016Article
- IL-1R1 is required for dendritic cell-mediated T cell reactivation within the CNS during West Nile virus encephalitis.The Journal of experimental medicine · 2013Article
- Interferon-gamma prevents death of bystander neurons during CD8 T cell responses in the brain.The American journal of pathology · 2009Article
- Antiviral CD8 T cells recognize borna disease virus antigen transgenically expressed in either neurons or astrocytes.Journal of virology · 2008Article
- Future trends in neurovirology: neuronal survival during virus infection and analysis of virus-specific T cells in central nervous system tissues.Journal of neurovirology · 2004Review
- Borna disease virus multiplication in mouse organotypic slice cultures is site-specifically inhibited by gamma interferon but not by interleukin-12.Journal of virology · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perforin-mediated lysis of target cells is the major antiviral effector mechanism of CD8(+) T lymphocytes. We have analyzed the role of perforin in a mouse model for CD8(+) T-cell-mediated central nervous system (CNS) immunopathology induced by Borna disease virus. When a defective perforin gene was introduced into the genetic background of the Borna disease-susceptible mouse strain MRL, the resulting perforin-deficient mice developed strong neurological disease in response to infection indistinguishable from that of their perforin-expressing littermates. The onset of disease was slightly delayed. Brains of diseased perforin-deficient mice showed similar amounts and a similar distribution of CD8(+) T cells as wild-type animals. Perforin deficiency had no impact on the kinetics of viral spread through the CNS. Unlike brain lymphocytes from diseased wild-type mice, lymphocytes from perforin-deficient MRL mice showed no in vitro cytolytic activity towards target cells expressing the nucleoprotein of Borna disease virus. Taken together, these results demonstrate that CD8(+) T cells mediate Borna disease independent of perforin. They further suggest that the pathogenic potential of CNS-infiltrating CD8(+) T cells does not primarily reside in their lytic activity but rather in other functions.
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