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Artículos de revistas sobre el tema "Borna"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 7 de febrero de 2022

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1

Hatalski, Carolyn. "Borna Disease". Emerging Infectious Diseases 3, n.º 2 (junio de 1997): 139–35. http://dx.doi.org/10.3201/eid0302.970205.

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2

Ferszt, R. y E. Severus. "Borna or not?" Pharmacopsychiatry 31, n.º 03 (mayo de 1998): 75–76. http://dx.doi.org/10.1055/s-2007-979304.

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3

Jordan, Ingo y W. Ian Lipkin. "Borna disease virus". Reviews in Medical Virology 11, n.º 1 (enero de 2001): 37–57. http://dx.doi.org/10.1002/rmv.300.

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4

Hornig, Mady, Thomas Briese y W. Ian Lipkin. "Borna Disease Virus". Journal of Neurovirology 9, n.º 2 (enero de 2003): 259–73. http://dx.doi.org/10.1080/13550280390194064.

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5

Amsterdam, Jay D. "Borna Disease Virus". Archives of General Psychiatry 42, n.º 11 (1 de noviembre de 1985): 1093. http://dx.doi.org/10.1001/archpsyc.1985.01790340077011.

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6

Malkinson, M., Y. Weisman, E. Ashash, L. Bode y H. Ludwig. "Borna disease in ostriches". Veterinary Record 133, n.º 12 (18 de septiembre de 1993): 304. http://dx.doi.org/10.1136/vr.133.12.304-b.

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7

Richt, Jürgen A., Arthur Grabner y Sibylle Herzog. "Borna Disease in Horses". Veterinary Clinics of North America: Equine Practice 16, n.º 3 (diciembre de 2000): 579–95. http://dx.doi.org/10.1016/s0749-0739(17)30097-4.

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8

Richt, J. A., A. Schmeel, K. Frese, K. M. Carbone, O. Narayan y R. Rott. "Borna disease virus-specific T cells protect against or cause immunopathological Borna disease." Journal of Experimental Medicine 179, n.º 5 (1 de mayo de 1994): 1467–73. http://dx.doi.org/10.1084/jem.179.5.1467.

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In this report we show that passive immunization of Lewis rats with viable CD4+, Borna disease virus (BDV)-specific T cells before infection with BDV resulted in protection against BD, whereas inoculation of these T cells after BDV infection induced clinical disease with more rapid onset than seen in BDV control animals. The protective as well as encephalitogenic effector functions of BDV-specific CD4+ T cells were mediated only by viable BDV-specific T cells. The protective situation was obtained by passive transfer of BDV-specific T cells into animals inoculated later with virus, whereas the immunopathological situation was observed when virus-specific T cells developed normally or after adoptive transfer, and appeared on the scene after considerable virus replication in the brain.
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9

Taieb, O., J. M. Baleyte, P. Mazet y A. M. Fillet. "Borna disease virus and psychiatry". European Psychiatry 16, n.º 1 (febrero de 2001): 3–10. http://dx.doi.org/10.1016/s0924-9338(00)00529-0.

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Borna disease virus (BDV), a noncytolytic neurotropic nonsegmented negative-stranded RNA virus with a wide geographic distribution, infects several vertebrate animal species and causes an immune-mediated central nervous system (CNS) disease with various manifestations, depending on both host and viral factors. In animal infections, BDV can persist in the CNS and induce alterations in brain cell functions, neurodevelopmental abnormalities and behavioral disturbances. An association between BDV and psychiatric disorders (essentially schizophrenia and affective disorders) has been suggested by some serologic and molecular studies but further investigations are required to substantiate the possible contribution of this virus to the pathogenesis of these disorders.
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10

Kerr, Cathel. "Borna disease virus and depression". Trends in Microbiology 9, n.º 9 (septiembre de 2001): 414. http://dx.doi.org/10.1016/s0966-842x(01)02197-7.

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11

Staeheli, Peter, Christian Sauder, Jürgen Hausmann, Felix Ehrensperger y Martin Schwemmle. "Epidemiology of Borna disease virus". Journal of General Virology 81, n.º 9 (1 de septiembre de 2000): 2123–35. http://dx.doi.org/10.1099/0022-1317-81-9-2123.

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12

Lieb, Klaus, Frank T. Hufert, Karl Bechter, Joachim Bauer y Johannes Kornhuber. "Depression, Borna disease, and amantadine". Lancet 349, n.º 9056 (marzo de 1997): 958. http://dx.doi.org/10.1016/s0140-6736(05)62741-9.

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13

Weissenbock, H., A. Suchy, P. Caplazi, S. Herzog y N. Nowotny. "Borna disease in Austrian horses". Veterinary Record 143, n.º 1 (4 de julio de 1998): 21–22. http://dx.doi.org/10.1136/vr.143.1.21.

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14

Lipkin, W. Ian, Kathryn M. Carbone, Michael C. Wilson, Cynthia S. Duchala, Opendra Narayan y Michael B. A. Oldstone. "Neurotransmitter abnormalities in Borna disease". Brain Research 475, n.º 2 (diciembre de 1988): 366–70. http://dx.doi.org/10.1016/0006-8993(88)90627-0.

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15

Taniyama, H., M. Okamoto, K. Hirayama, K. Hagiwara, R. Kirisawa, K. Tsunoda, W. Kamitani y K. Ikuta. "Equine Borna disease in Japan". Veterinary Record 148, n.º 15 (14 de abril de 2001): 480–82. http://dx.doi.org/10.1136/vr.148.15.480.

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16

Waelchli, R., F. Ehrensperger, A. Metzler y C. Winder. "Borna disease in a sheep". Veterinary Record 117, n.º 19 (9 de noviembre de 1985): 499–500. http://dx.doi.org/10.1136/vr.117.19.499.

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17

Igata, Tomohide, Kazunari Yamaguchi, Ruriko Igata-Yi, Keiko Yoshiki, Shigeki Takemoto, Hiroshi Yamasaki, Masao Matuoka y Taihei Miyakawa. "Dementia and Borna Disease Virus". Dementia and Geriatric Cognitive Disorders 9, n.º 1 (19 de diciembre de 1997): 24–25. http://dx.doi.org/10.1159/000017017.

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18

Waltrip, Royce W., Robert W. Buchanan, Ann Summerfelt, Alan Breier, William T. Carpenter, Nancy L. Bryant, Steven A. Rubin y Kathryn M. Carbone. "Borna disease virus and schizophrenia". Psychiatry Research 56, n.º 1 (enero de 1995): 33–44. http://dx.doi.org/10.1016/0165-1781(94)02600-n.

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19

Pelle, M., R. C. Alexander, Z. F. Fu, B. Dietzschold y H. Koprowski. "Borna disease antibodies in schizophrenia". Schizophrenia Research 15, n.º 1-2 (abril de 1995): 189. http://dx.doi.org/10.1016/0920-9964(95)95582-t.

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20

Solbrig, Marylou V. "Animal Models of CNS Viral Disease: Examples from Borna Disease Virus Models". Interdisciplinary Perspectives on Infectious Diseases 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/709791.

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Borna disease (BD), caused by the neurotropic RNA virus, Borna Disease virus, is an affliction ranging from asymptomatic to fatal meningoencephalitis across naturally and experimentally infected warmblooded (mammalian and bird) species. More than 100 years after the first clinical descriptions of Borna disease in horses and studies beginning in the 1980's linking Borna disease virus to human neuropsychiatric diseases, experimentally infected rodents have been used as models for examining behavioral, neuropharmacological, and neurochemical responses to viral challenge at different stages of life. These studies have contributed to understanding the role of CNS viral injury in vulnerability to behavioral, developmental, epileptic, and neurodegenerative diseases and aided evaluation of the proposed and still controversial links to human disease.
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21

Oldach, D., M. C. Zink, J. M. Pyper, S. Herzog, R. Rott, O. Narayan y J. E. Clements. "Induction of protection against Borna disease by inoculation with high-dose-attenuated Borna disease virus". Virology 206, n.º 1 (enero de 1995): 426–34. http://dx.doi.org/10.1016/s0042-6822(95)80058-1.

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22

Lewis, Ann J., J. Lindsay Whitton, Carolyn G. Hatalski, Herbert Weissenböck y W. Ian Lipkin. "Effect of Immune Priming on Borna Disease". Journal of Virology 73, n.º 3 (1 de marzo de 1999): 2541–46. http://dx.doi.org/10.1128/jvi.73.3.2541-2546.1999.

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ABSTRACT Borna disease virus (BDV) is a neurotropic virus with a broad host and geographic range. Lewis rats were immunized against BDV with a recombinant vaccinia virus expressing the BDV nucleoprotein and were later infected with BDV to evaluate protection against Borna disease (BD). Relative to animals that were not immunized, immunized animals had a decreased viral burden after challenge with infectious virus, more marked inflammation, and aggravated clinical disease. These data suggest that a more robust immune response in Borna disease can reduce viral load at the expense of increased morbidity.
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23

Bode, L., D. E. Dietrich y H. Ludwig. "Depression and Borna disease virus (BDV)". European Psychiatry 17 (mayo de 2002): 32. http://dx.doi.org/10.1016/s0924-9338(02)80145-6.

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24

Sturm, Vinzent y Helge Beuermann. "Die geotechnische Sanierung des Speichers Borna". WASSERWIRTSCHAFT 109, n.º 5 (mayo de 2019): 30–33. http://dx.doi.org/10.1007/s35147-019-0034-6.

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25

Rott, R., S. Herzog, J. Richt y L. Stitz. "Immune-Mediated Pathogenesis of Borna Disease". Zentralblatt für Bakteriologie, Mikrobiologie und Hygiene. Series A: Medical Microbiology, Infectious Diseases, Virology, Parasitology 270, n.º 1-2 (noviembre de 1988): 295–301. http://dx.doi.org/10.1016/s0176-6724(88)80166-4.

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26

Caplazi, P., A. Waldvogel, L. Stitz, U. Braun y F. Ehrensperger. "Borna disease in naturally infected cattle". Journal of Comparative Pathology 111, n.º 1 (julio de 1994): 65–72. http://dx.doi.org/10.1016/s0021-9975(05)80112-4.

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27

Lipkin, W. Ian, Thomas Briese y Mady Hornig. "Borna disease virus – Fact and fantasy". Virus Research 162, n.º 1-2 (diciembre de 2011): 162–72. http://dx.doi.org/10.1016/j.virusres.2011.09.036.

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28

Gonzalez–Dunia, Daniel, Christian Sauder y Juan Carlos de la Torre. "Borna Disease Virus and the Brain". Brain Research Bulletin 44, n.º 6 (enero de 1997): 647–64. http://dx.doi.org/10.1016/s0361-9230(97)00276-1.

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29

Lebain, Pierrick, Astrid Vabret, Perrine Brazo, Benoı̂t Chabot, François Freymuth y Sonia Dollfus. "Borna disease virus and psychiatric disorders". Schizophrenia Research 57, n.º 2-3 (octubre de 2002): 303–5. http://dx.doi.org/10.1016/s0920-9964(01)00317-6.

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30

Briese, T., A. Schneemann, A. J. Lewis, Y. S. Park, S. Kim, H. Ludwig y W. I. Lipkin. "Genomic organization of Borna disease virus." Proceedings of the National Academy of Sciences 91, n.º 10 (10 de mayo de 1994): 4362–66. http://dx.doi.org/10.1073/pnas.91.10.4362.

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31

Kim, Yong-Ku, Sang-Hyun Kim, Chang-Su Han, Heon-Jeong Lee, Hyung-Seob Kim, Sung-Chul Yoon, Dai-Jin Kim, Ki-Joon Song, Michael Maes y Jin-Won Song. "Borna disease virus and deficit schizophrenia". Acta Neuropsychiatrica 15, n.º 5 (octubre de 2003): 262–65. http://dx.doi.org/10.1034/j.1601-5215.2003.00043.x.

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Background:It is controversial whether Borna disease virus (BDV) infects humans and causes psychiatric disorders.Objectives:The relationship between BDV infection and schizophrenia with deficit syndrome was investigated.Study design:Using the Schedule for the Deficit Syndrome, 62 schizophrenic in-patients were selected from three psychiatric hospitals. RNA was extracted from peripheral blood mononuclear cells and analyzed using nested reverse transcriptase-polymerase chain reaction with primers to detect BDV p24 and p40.Results and conclusions:BDV transcripts were not detected in samples from any of the 62 schizophrenic patients. These data do not support an etiologic association between BDV infection and the deficit form of schizophrenia.
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32

Pyper, Joanna M. "Does Borna disease virus infect humans?" Nature Medicine 1, n.º 3 (marzo de 1995): 209–10. http://dx.doi.org/10.1038/nm0395-209.

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33

Wensman, Jonas Johansson, Karin Hultin Jäderlund, Bodil Ström Holst y Mikael Berg. "Borna disease virus infection in cats". Veterinary Journal 201, n.º 2 (agosto de 2014): 142–49. http://dx.doi.org/10.1016/j.tvjl.2013.12.012.

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34

Haga, S., Y. Motoi y K. Ikeda. "Borna disease virus and neuropsychiatric disorders". Lancet 350, n.º 9077 (agosto de 1997): 592–93. http://dx.doi.org/10.1016/s0140-6736(05)63183-2.

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35

Nowotny, Norbert y Johann Windhaber. "Borna disease virus and neuropsychiatric disorders". Lancet 350, n.º 9077 (agosto de 1997): 593. http://dx.doi.org/10.1016/s0140-6736(05)63184-4.

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36

Carbone, K. M. y M. V. Pletnikov. "Borna again, starting from the beginning". Molecular Psychiatry 5, n.º 6 (noviembre de 2000): 577. http://dx.doi.org/10.1038/sj.mp.4000810.

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37

Carbone, Kathryn M. "Borna Disease Virus and Human Disease". Clinical Microbiology Reviews 14, n.º 3 (1 de julio de 2001): 513–27. http://dx.doi.org/10.1128/cmr.14.3.513-527.2001.

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SUMMARY The biology of Borna disease virus (BDV) strongly supports the likelihood of human infection with BDV or a variant of BDV. Thus far, the evidence supporting BDV infection in humans has initiated much controversy among basic and clinical scientists; only time and additional research will support or refute the hypothesis of human BDV infection. Until an assay of acceptable specificity and sensitivity has been developed, validated, and used to document human BDV infection, scientists cannot reasonably begin to associate BDV infection with specific disease syndromes. Clinical studies seeking causal associations between BDV infection and specific diseases must ensure the proper identification of the BDV infection status of patients and control subjects by using a validated, highly sensitive, and highly specific assay (or series of assays). For clinical studies, a highly sensitive “screening” test followed by a highly specific confirmatory test will be of significant benefit. Although it is possible to formulate hypotheses about the clinical outcomes of human BDV infection based on animal model work, to date no human disease has been causally linked to human BDV infection. Scientists all over the world are actively pursuing these issues, and with continuing advances in clinical and basic BDV research, the answers cannot be far away.
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38

Lutz, Hans, Diane D. Addie, Corine Boucraut-Baralon, Herman Egberink, Tadeusz Frymus, Tim Gruffydd-Jones, Katrin Hartmann et al. "Borna disease virus infection in cats". Journal of Feline Medicine and Surgery 17, n.º 7 (22 de junio de 2015): 614–16. http://dx.doi.org/10.1177/1098612x15588452.

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39

TANIYAMA, Hiroyuki. "Borna Disease of Animals in Japan". Journal of the Japan Veterinary Medical Association 54, n.º 1 (2001): 1–6. http://dx.doi.org/10.12935/jvma1951.54.1.

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40

Clarkson, Sheilagh. "Reverse genetics for Borna disease virus". Nature Reviews Microbiology 1, n.º 3 (diciembre de 2003): 174. http://dx.doi.org/10.1038/nrmicro790.

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41

Waltrip, R. W., R. W. Buchanan, A. Summerfelt, A. Breier, W. T. Carpenter, N. L. Bryant, B. Kirkpatrick, S. A. Rubin y K. M. Carbone. "Borna disease virus antibodies and schizophrenia". Schizophrenia Research 15, n.º 1-2 (abril de 1995): 73. http://dx.doi.org/10.1016/0920-9964(95)95231-w.

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42

Eickmann, Markus, Simone Kiermayer, Ina Kraus, Melanie Gössl, Jürgen A. Richt y Wolfgang Garten. "Maturation of Borna disease virus glycoprotein". FEBS Letters 579, n.º 21 (8 de agosto de 2005): 4751–56. http://dx.doi.org/10.1016/j.febslet.2005.07.052.

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43

Tesfaye, Ashenafi y Klaus Wedekind. "Characteristics of Omotic tone Shinasha Borna". Studies in African Linguistics 21, n.º 3 (1 de diciembre de 1990): 347–68. http://dx.doi.org/10.32473/sal.v21i3.107432.

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The article provides some phonological background and outlines the tonal system of Shinasha (Borna), an isolated North Omotic language of Ethiopia. There are two contrasting tones. Their behaviour shows characteristics which have also been observed for other Omotic languages: stability of lexical tone, limited use of tone in the syntax, and absence of sandhi. The article provides new evidence that vowel quality can have a strong influence on the tonetic realisation: Shinasha is not the only Omotic language where high vowel quality is associated with extra high pitch.
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44

Henkel, Marco, Oliver Planz, Timo Fischer, Lothar Stitz y Hanns-Joachim Rziha. "Prevention of Virus Persistence and Protection against Immunopathology after Borna Disease Virus Infection of the Brain by a Novel Orf Virus Recombinant". Journal of Virology 79, n.º 1 (1 de enero de 2005): 314–25. http://dx.doi.org/10.1128/jvi.79.1.314-325.2005.

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ABSTRACT The Parapoxvirus Orf virus represents a promising candidate for novel vector vaccines due to its immune modulating properties even in nonpermissive hosts such as mouse or rat. The highly attenuated Orf virus strain D1701 was used to generate a recombinant virus (D1701-VrVp40) expressing nucleoprotein p40 of Borna disease virus, which represents a major antigen for the induction of a Borna disease virus-specific humoral and cellular immune response. Infection with Borna disease virus leads to distinct neurological symptoms mediated by the invasion of activated specific CD8+ T cells into the infected brain. Usually, Borna disease virus is not cleared from the brain but rather persists in neural cells. In the present study we show for the first time that intramuscular application of the D1701-VrVp40 recombinant protected rats against Borna disease, and importantly, virus clearance from the infected brain was demonstrated in immunized animals. Even 4 and 8 months after the last immunization, all immunized animals were still protected against the disease. Initial characterization of the immune cells attracted to the infected brain areas suggested that D1701-VrVp40 mediated induction of B cells and antibody-producing plasma cells as well as T cells. These findings suggest the induction of various defense mechanisms against Borna disease virus. First studies on the role of antiviral cytokines indicated that D1701-VrVp40 immunization did not lead to an enhanced early response of gamma or alpha interferon or tumor necrosis factor alpha. Collectively, this study describes the potential of the Orf virus vector system in mediating long-lasting, protective antiviral immunity and eliminating this persistent virus infection without provoking massive neuronal damage.
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45

Degiorgis, M. P., A. L. Berg, C. Hård af Segerstad, T. Mörner, M. Johansson y M. Berg. "Borna Disease in a Free-Ranging Lynx (Lynx lynx)". Journal of Clinical Microbiology 38, n.º 8 (2000): 3087–91. http://dx.doi.org/10.1128/jcm.38.8.3087-3091.2000.

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A free-ranging lynx (Lynx lynx) was shot because of its abnormal behavior. Histopathological examination revealed a nonsuppurative meningoencephalitis. In situ hybridization, immunohistochemistry, and reverse transcriptase PCR analysis showed the presence of Borna disease virus infection in the brain. To our knowledge, this is the first confirmed case of Borna disease in a large felid.
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46

Hausmann, Jürgen, Karin Schamel y Peter Staeheli. "CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin". Journal of Virology 75, n.º 21 (1 de noviembre de 2001): 10460–66. http://dx.doi.org/10.1128/jvi.75.21.10460-10466.2001.

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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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47

Ikuta, Kazuyoshi. "Borna disease virus and infection in humans". Frontiers in Bioscience 7, n.º 1-3 (2002): d470. http://dx.doi.org/10.2741/ikuta.

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48

Stitz, Lothar. "The immunopathogenesis of Borna disease virus infection". Frontiers in Bioscience 7, n.º 1-3 (2002): d541. http://dx.doi.org/10.2741/stitz.

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49

Berg, A. L. y M. Berg. "A variant form of feline borna disease". Journal of Comparative Pathology 119, n.º 3 (octubre de 1998): 323–31. http://dx.doi.org/10.1016/s0021-9975(98)80054-6.

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50

Waltrip, R. W., R. W. Buchanan, K. M. Carbone, A. Breier, O. Narayan y W. T. Carpenter. "Borna disease virus and schizophrenia: Preliminary results". Schizophrenia Research 4, n.º 3 (mayo de 1991): 374. http://dx.doi.org/10.1016/0920-9964(91)90305-b.

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