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Journal articles on the topic 'Virus de la maladie de Borna'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2025

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1

Brugère-Picoux, Jeanne, Lise Bode, Antoine Del Sole, and Hans Ludwig. "Identification du virus de la maladie de Borna en France." Bulletin de l'Académie Vétérinaire de France, no. 1 (2000): 411. http://dx.doi.org/10.4267/2042/62761.

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2

Scordel, Chloé, and Muriel Coulpier. "La phosphoprotéine P du virus de la maladie de Borna altère le développement des neurones GABAergiques humains." médecine/sciences 31, no. 12 (December 2015): 1060–63. http://dx.doi.org/10.1051/medsci/20153112003.

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3

Hornig, Mady, Thomas Briese, and W. Ian Lipkin. "Borna Disease Virus." Journal of Neurovirology 9, no. 2 (January 2003): 259–73. http://dx.doi.org/10.1080/13550280390194064.

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4

Jordan, Ingo, and W. Ian Lipkin. "Borna disease virus." Reviews in Medical Virology 11, no. 1 (January 2001): 37–57. http://dx.doi.org/10.1002/rmv.300.

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5

Amsterdam, Jay D. "Borna Disease Virus." Archives of General Psychiatry 42, no. 11 (November 1, 1985): 1093. http://dx.doi.org/10.1001/archpsyc.1985.01790340077011.

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6

Henkel, Marco, Oliver Planz, Timo Fischer, Lothar Stitz, and 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, no. 1 (January 1, 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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7

Kerr, Cathel. "Borna disease virus and depression." Trends in Microbiology 9, no. 9 (September 2001): 414. http://dx.doi.org/10.1016/s0966-842x(01)02197-7.

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8

Taieb, O., J. M. Baleyte, P. Mazet, and A. M. Fillet. "Borna disease virus and psychiatry." European Psychiatry 16, no. 1 (February 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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9

Waltrip, Royce W., Robert W. Buchanan, Ann Summerfelt, Alan Breier, William T. Carpenter, Nancy L. Bryant, Steven A. Rubin, and Kathryn M. Carbone. "Borna disease virus and schizophrenia." Psychiatry Research 56, no. 1 (January 1995): 33–44. http://dx.doi.org/10.1016/0165-1781(94)02600-n.

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10

Staeheli, Peter, Christian Sauder, Jürgen Hausmann, Felix Ehrensperger, and Martin Schwemmle. "Epidemiology of Borna disease virus." Journal of General Virology 81, no. 9 (September 1, 2000): 2123–35. http://dx.doi.org/10.1099/0022-1317-81-9-2123.

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11

Igata, Tomohide, Kazunari Yamaguchi, Ruriko Igata-Yi, Keiko Yoshiki, Shigeki Takemoto, Hiroshi Yamasaki, Masao Matuoka, and Taihei Miyakawa. "Dementia and Borna Disease Virus." Dementia and Geriatric Cognitive Disorders 9, no. 1 (December 19, 1997): 24–25. http://dx.doi.org/10.1159/000017017.

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12

Lewis, Ann J., J. Lindsay Whitton, Carolyn G. Hatalski, Herbert Weissenböck, and W. Ian Lipkin. "Effect of Immune Priming on Borna Disease." Journal of Virology 73, no. 3 (March 1, 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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13

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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14

Stitz, L., O. Planz, T. Bilzer, K. Frei, and A. Fontana. "Transforming growth factor-beta modulates T cell-mediated encephalitis caused by Borna disease virus. Pathogenic importance of CD8+ cells and suppression of antibody formation." Journal of Immunology 147, no. 10 (November 15, 1991): 3581–86. http://dx.doi.org/10.4049/jimmunol.147.10.3581.

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Abstract Borna disease is a virus-induced, immune-mediated encephalomyelitis based on a delayed-type hypersensitivity reaction. The severity of clinical symptoms after intracerebral infection of rats with Borna disease virus was reduced after treatment with transforming growth factor (TGF-beta 2). Intraperitoneal injection of the recombinant molecule, rTGF-beta 2, started on the day of infection at a dose of either 1 micrograms given every day or every other day for 8 consecutive days or 2 micrograms every third day, was found to result in the absence of typical Borna disease symptoms at 14 days after infection in most of the TGF-beta-treated rats, a time point at which all infected control animals not treated with rTGF-beta 2 showed distinct signs of Borna disease. The inhibition of the disease was paralleled by a significant reduction of the inflammatory reaction in the brain. However, the efficacy of treatment with rTGF-beta 2 was transient, because after day 21 only a slight or no reduction of the inflammatory reaction and, consequently, symptoms of Borna disease could be observed. Immunohistologic investigations revealed reduced CD4+ T cell numbers and no changes in macrophage counts in encephalitic lesions of rTG-beta treated rats. However, CD8+ cells were markedly decreased in the encephalitic lesions. Furthermore, the expression of MHC class II Ag was significantly reduced in the brain of rTGF-beta 2 treated Borna disease virus-infected rats, whereas MHC class I Ag expression was not. Most treated animals showed a reduction of Borna disease virus-specific serum antibodies, the result of an inhibition of the IgG response. The results presented here suggest a distinct influence of rTGF-beta 2 on T cell-mediated immune functions during the early phase of Borna disease virus-induced encephalomyelitis.

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15

Richt, J. A., A. Schmeel, K. Frese, K. M. Carbone, O. Narayan, and R. Rott. "Borna disease virus-specific T cells protect against or cause immunopathological Borna disease." Journal of Experimental Medicine 179, no. 5 (May 1, 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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16

Clarkson, Sheilagh. "Reverse genetics for Borna disease virus." Nature Reviews Microbiology 1, no. 3 (December 2003): 174. http://dx.doi.org/10.1038/nrmicro790.

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17

Carbone, Kathryn M. "Borna Disease Virus and Human Disease." Clinical Microbiology Reviews 14, no. 3 (July 1, 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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18

Pyper, Joanna M. "Does Borna disease virus infect humans?" Nature Medicine 1, no. 3 (March 1995): 209–10. http://dx.doi.org/10.1038/nm0395-209.

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19

Briese, T., A. Schneemann, A. J. Lewis, Y. S. Park, S. Kim, H. Ludwig, and W. I. Lipkin. "Genomic organization of Borna disease virus." Proceedings of the National Academy of Sciences 91, no. 10 (May 10, 1994): 4362–66. http://dx.doi.org/10.1073/pnas.91.10.4362.

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20

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, and Jin-Won Song. "Borna disease virus and deficit schizophrenia." Acta Neuropsychiatrica 15, no. 5 (October 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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21

Lipkin, W. Ian, Thomas Briese, and Mady Hornig. "Borna disease virus – Fact and fantasy." Virus Research 162, no. 1-2 (December 2011): 162–72. http://dx.doi.org/10.1016/j.virusres.2011.09.036.

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22

Gonzalez–Dunia, Daniel, Christian Sauder, and Juan Carlos de la Torre. "Borna Disease Virus and the Brain." Brain Research Bulletin 44, no. 6 (January 1997): 647–64. http://dx.doi.org/10.1016/s0361-9230(97)00276-1.

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23

Lebain, Pierrick, Astrid Vabret, Perrine Brazo, Benoı̂t Chabot, François Freymuth, and Sonia Dollfus. "Borna disease virus and psychiatric disorders." Schizophrenia Research 57, no. 2-3 (October 2002): 303–5. http://dx.doi.org/10.1016/s0920-9964(01)00317-6.

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24

Wensman, Jonas Johansson, Karin Hultin Jäderlund, Bodil Ström Holst, and Mikael Berg. "Borna disease virus infection in cats." Veterinary Journal 201, no. 2 (August 2014): 142–49. http://dx.doi.org/10.1016/j.tvjl.2013.12.012.

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25

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

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26

Haga, S., Y. Motoi, and K. Ikeda. "Borna disease virus and neuropsychiatric disorders." Lancet 350, no. 9077 (August 1997): 592–93. http://dx.doi.org/10.1016/s0140-6736(05)63183-2.

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27

Nowotny, Norbert, and Johann Windhaber. "Borna disease virus and neuropsychiatric disorders." Lancet 350, no. 9077 (August 1997): 593. http://dx.doi.org/10.1016/s0140-6736(05)63184-4.

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28

Waltrip, R. W., R. W. Buchanan, A. Summerfelt, A. Breier, W. T. Carpenter, N. L. Bryant, B. Kirkpatrick, S. A. Rubin, and K. M. Carbone. "Borna disease virus antibodies and schizophrenia." Schizophrenia Research 15, no. 1-2 (April 1995): 73. http://dx.doi.org/10.1016/0920-9964(95)95231-w.

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29

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, no. 7 (June 22, 2015): 614–16. http://dx.doi.org/10.1177/1098612x15588452.

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30

Eickmann, Markus, Simone Kiermayer, Ina Kraus, Melanie Gössl, Jürgen A. Richt, and Wolfgang Garten. "Maturation of Borna disease virus glycoprotein." FEBS Letters 579, no. 21 (August 8, 2005): 4751–56. http://dx.doi.org/10.1016/j.febslet.2005.07.052.

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31

Hausmann, Jürgen, Karin Schamel, and Peter Staeheli. "CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin." Journal of Virology 75, no. 21 (November 1, 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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32

Ikuta, Kazuyoshi. "Borna disease virus and infection in humans." Frontiers in Bioscience 7, no. 1-3 (2002): d470. http://dx.doi.org/10.2741/ikuta.

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33

Stitz, Lothar. "The immunopathogenesis of Borna disease virus infection." Frontiers in Bioscience 7, no. 1-3 (2002): d541. http://dx.doi.org/10.2741/stitz.

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34

Ludwig, Hanns, and Liv Bode. "The Neuropathogenesis of Borna Disease Virus Infections." Intervirology 40, no. 2-3 (1997): 185–97. http://dx.doi.org/10.1159/000150545.

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35

SCHOLBACH, THOMAS, and LIV BODE. "Borna Disease Virus infection in young children." APMIS 116 (June 2008): 83–88. http://dx.doi.org/10.1111/j.1600-0463.2008.00m16.x.

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36

Thierer, J., H. Riehle, O. Grebenstein, T. Binz, S. Herzog, N. Thiedemann, L. Stitz, R. Rott, F. Lottspeich, and H. Niemann. "The 24K protein of Borna disease virus." Journal of General Virology 73, no. 2 (February 1, 1992): 413–16. http://dx.doi.org/10.1099/0022-1317-73-2-413.

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37

Gonzalez-Dunia, Daniel, Romain Volmer, Daniel Mayer, and Martin Schwemmle. "Borna disease virus interference with neuronal plasticity." Virus Research 111, no. 2 (August 2005): 224–34. http://dx.doi.org/10.1016/j.virusres.2005.04.011.

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38

Ferszt, R., E. Severus, L. Bode, M. Brehm, K. P. Kühl, H. Berzewski, and H. Ludwig. "Activated Borna Disease Virus in Affective Disorders." Pharmacopsychiatry 32, no. 03 (May 1999): 93–98. http://dx.doi.org/10.1055/s-2007-979201.

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39

Volmer, Romain, Christine M. A. Prat, Gwendal Le Masson, André Garenne, and Daniel Gonzalez-Dunia. "Borna Disease Virus Infection Impairs Synaptic Plasticity." Journal of Virology 81, no. 16 (June 6, 2007): 8833–37. http://dx.doi.org/10.1128/jvi.00612-07.

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ABSTRACT The mechanisms whereby Borna disease virus (BDV) can impair neuronal function and lead to neurobehavioral disease are not well understood. To analyze the electrophysiological properties of neurons infected with BDV, we used cultures of neurons grown on multielectrode arrays, allowing a real-time monitoring of the electrical activity across the network shaped by synaptic transmission. Although infection did not affect spontaneous neuronal activity, it selectively blocked activity-dependent enhancement of neuronal network activity, one form of synaptic plasticity thought to be important for learning and memory. These findings highlight the original mechanism of the neuronal dysfunction caused by noncytolytic infection with BDV.

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40

Carbone, K. "Borna disease: virus-induced neurobehavioral disease pathogenesis." Current Opinion in Microbiology 4, no. 4 (August 1, 2001): 467–75. http://dx.doi.org/10.1016/s1369-5274(00)00237-x.

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41

Waltrip, Royce W., Jeffrey Lieberman, Delbert Robinson, Robert M. Bilder, Jose M. Alvir, Lisa R. King, Ann Summerfelt, Steven A. Rubin, and Kathryn M. Carbone. "First episode schizophrenia and borna disease virus." Schizophrenia Research 24, no. 1-2 (January 1997): 261. http://dx.doi.org/10.1016/s0920-9964(97)82754-5.

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42

Hewson, Roger. "Borna disease virus takes the acid test." Molecular Medicine Today 4, no. 4 (April 1998): 142. http://dx.doi.org/10.1016/s1357-4310(98)01218-0.

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43

de la Torre, Juan Carlos, Liv Bode, Ralf Dürrwald, Beatrice Cubitt, and Hanns Ludwig. "Sequence characterization of human Borna disease virus." Virus Research 44, no. 1 (September 1996): 33–44. http://dx.doi.org/10.1016/0168-1702(96)01338-x.

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44

Ikuta, Kazuyoshi. "Borna disease virus and infection in humans." Frontiers in Bioscience 7, no. 4 (2002): d470–495. http://dx.doi.org/10.2741/a789.

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45

Stitz, Lothar. "The immunopathogenesis of Borna disease virus infection." Frontiers in Bioscience 7, no. 4 (2002): d541–555. http://dx.doi.org/10.2741/a793.

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46

Waltrip, R. W., R. W. Buchanan, K. M. Carbone, A. Breier, O. Narayan, and W. T. Carpenter. "Borna disease virus and schizophrenia: Preliminary results." Schizophrenia Research 4, no. 3 (May 1991): 374. http://dx.doi.org/10.1016/0920-9964(91)90305-b.

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47

Poenisch, Marion, Gunhild Unterstab, Thorsten Wolff, Peter Staeheli, and Urs Schneider. "The X protein of Borna disease virus regulates viral polymerase activity through interaction with the P protein." Journal of General Virology 85, no. 7 (July 1, 2004): 1895–98. http://dx.doi.org/10.1099/vir.0.80002-0.

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Borna disease virus polymerase activity is negatively regulated by the viral X protein. Using a virus minireplicon system it was found that all X mutants that no longer interacted with the viral P protein failed to exhibit significant inhibitory activity. The action of X could further be neutralized by expression of a P fragment that contained the X interaction domain but lacked all domains known to mediate interaction with other viral proteins. X thus appears to regulate the activity of the Borna disease virus polymerase by targeting the polymerase cofactor P.

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48

Kinnunen, Paula M., Airi Palva, Antti Vaheri, and Olli Vapalahti. "Epidemiology and host spectrum of Borna disease virus infections." Journal of General Virology 94, no. 2 (February 1, 2013): 247–62. http://dx.doi.org/10.1099/vir.0.046961-0.

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Borna disease virus (BDV) has gained lot of interest because of its zoonotic potential, ability to introduce cDNA of its RNA transcripts into host genomes, and ability to cause severe neurobehavioural diseases. Classical Borna disease is a progressive meningoencephalomyelitis in horses and sheep, known in central Europe for centuries. According to current knowledge, BDV or a close relative also infects several other species, including humans at least occasionally, in central Europe and elsewhere, but the existence of potential ‘human Borna disease’ with its suspected neuropsychiatric symptoms is highly controversial. The recent detection of endogenized BDV-like genes in primate and various other vertebrate genomes confirms that at least ancient bornaviruses did infect our ancestors. The epidemiology of BDV is largely unknown, but accumulating evidence indicates vectors and reservoirs among small wild mammals. The aim of this review is to bring together the current knowledge on epidemiology of BDV infections. Specifically, geographical and host distribution are addressed and assessed in the critical light of the detection methods used. We also review some salient clinical aspects.

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49

Kasenga, By Fyson. "Corona Virus Pandemic: A Case of Prevention in Rural Malawi." Clinical Research Notes 3, no. 4 (May 23, 2022): 01–04. http://dx.doi.org/10.31579/2690-8816/067.

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Covid-19 has brought untold harm and human suffering worldwide. Deaths and economic recessions continue to increase in many countries of the world particularly in European countries. In the recent past, Africa presented itself as less affected than the rest of the world but now the situation is changing dramatically. An intervention study was done in two districts of rural Malawi namely Thyolo and Mulanje to reduce infection rate of covid-19. Ten villages comprising of 852 households were included in the study. Personal protective equipment Resources (PPEs) coupled with preventive messages with an emphasis on hand washing, distancing, wearing of face masks and contact tracing were mainly the content of the messages. Washing buckets with taps, basins and soaps were provided in groups. The villages were followed up six months later and established that diarrhoea diseases reduced among the under-fives and in the adult population. The findings of the study concluded that as communities adhered to the prevention measures of covid-19, other diseases related to poor sanitation reduced in the studied population. Based on the study findings, it is recommended to increase the study population and resources for the prevention of covid-19 disease to yield positive domain effect. Conducting a country wide similar study would be beneficial and need to be considered which will prevent the general population from covid-19 and other water borne diseases.

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50

Degiorgis, M. P., A. L. Berg, C. Hård af Segerstad, T. Mörner, M. Johansson, and M. Berg. "Borna Disease in a Free-Ranging Lynx (Lynx lynx)." Journal of Clinical Microbiology 38, no. 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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