Diabolical effects of rabies encephalitis
详细信息    查看全文
  • 作者:Alan C. Jackson
  • 关键词:Aggressive behavior ; Mitochondrial dysfunction ; Oxidative stress ; Pathogenesis ; Rabies ; Serotonin ; Viral encephalitis
  • 刊名:Journal of NeuroVirology
  • 出版年:2016
  • 出版时间:February 2016
  • 年:2016
  • 卷:22
  • 期:1
  • 页码:8-13
  • 全文大小:696 KB
  • 参考文献:Alandijany T, Kammouni W, Roy Chowdhury SK, Fernyhough P, Jackson AC (2013) Mitochondrial dysfunction in rabies virus infection of neurons. J Neurovirol 19:537–549PubMed CrossRef
    Charlton KM, Casey GA, Campbell JB (1984) Experimental rabies in skunks: effects of immunosuppression induced by cyclophosphamide. Can J Comp Med 48:72–77PubMed PubMedCentral
    Derry CP, Wilkie MD, Al-Shahi SR, Davenport RJ (2011) Autoimmune limbic encephalitis. Clin Med 11:476–478CrossRef
    Fato R, Bergamini C, Leoni S, Strocchi P, Lenaz G (2008) Generation of reactive oxygen species by mitochondrial complex I: implications in neurodegeneration. Neurochem Res 33:2487–2501PubMed CrossRef
    Feng G, Mellor RH, Bernstein M, Keller-Peck C, Nguyen QT, Wallace M, Nerbonne JM, Lichtman JW, Sanes JR (2000) Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP. Neuron 28:41–51PubMed CrossRef
    Fu ZF, Jackson AC (2005) Neuronal dysfunction and death in rabies virus infection. J Neurovirol 11:101–106PubMed CrossRef
    Hanlon CA (2013) Rabies in terrestrial animals. In: Jackson AC (ed) Rabies: scientific basis of the disease and its management, 3rd edn. Elsevier Academic Press, Oxford, pp 179–213CrossRef
    Irwin MH, Parameshwaran K, Pinkert CA (2013) Mouse models of mitochondrial complex I dysfunction. Int J Biochem Cell Biol 45:34–40PubMed PubMedCentral CrossRef
    Isaacson RL (1989) The neural and behavioural mechanisms of aggression and their alteration by rabies and other viral infections. In: Thraenhart O, Koprowski H, Bögel K, Sureau P (eds) Progress in rabies control: proceedings of the Second International IMVI ESSEN/WHO Symposium on “New Developments in Rabies Control”, Essen, 5–7 July 1988; and Report of the WHO Consultation on Rabies, Essen, 8 July 1988 WHO Consultation on Rabies. Wells Medical, Royal Tunbridge Wells, Kent, pp 17–23
    Jackson AC (2013) Human disease. In: Jackson AC (ed) Rabies: scientific basis of the disease and its management, 3rd edn. Elsevier Academic Press, Oxford, pp 269–298CrossRef
    Jackson AC, Fu ZF (2013) Pathogenesis. In: Jackson AC (ed) Rabies: scientific basis of the disease and its management, 3rd edn. Elsevier Academic Press, Oxford, pp 299–349CrossRef
    Jackson AC, Kammouni W, Zherebitskaya E, Fernyhough P (2010) Role of oxidative stress in rabies virus infection of adult mouse dorsal root ganglion neurons. J Virol 84:4697–4705PubMed PubMedCentral CrossRef
    Johnson RT (1971) The pathogenesis of experimental rabies. In: Nagano Y, Davenport FM (eds) Rabies. University Park Press, Baltimore, pp 59–75
    Kalin NH (1999) Primate models to understand human aggression. J Clin Psychiatry 60(Suppl 15):29–32PubMed
    Kammouni W, Wood H, Saleh A, Appolinario CM, Fernyhough P, Jackson AC (2015) Rabies virus phosphoprotein interacts with mitochondrial complex I and induces mitochondrial dysfunction and oxidative stress. J Neurovirol (in press)
    Lauria G, Morbin M, Lombardi R, Borgna M, Mazzoleni G, Sghirlanzoni A, Pareyson D (2003) Axonal swellings predict the degeneration of epidermal nerve fibers in painful neuropathies. Neurology 61:631–636PubMed CrossRef
    Li XQ, Sarmento L, Fu ZF (2005) Degeneration of neuronal processes after infection with pathogenic, but not attenuated, rabies viruses. J Virol 79:10063–10068PubMed PubMedCentral CrossRef
    Murphy MP (2009) How mitochondria produce reactive oxygen species. Biochem J 417:1–13PubMed PubMedCentral CrossRef
    Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M (2000) Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature 404:787–790PubMed CrossRef
    Obrosova IG, Van HC, Fathallah L, Cao XC, Greene DA, Stevens MJ (2002) An aldose reductase inhibitor reverses early diabetes-induced changes in peripheral nerve function, metabolism, and antioxidative defense. FASEB J 16:123–125PubMed
    Obrosova IG, Pacher P, Szabo C, Zsengeller Z, Hirooka H, Stevens MJ, Yorek MA (2005) Aldose reductase inhibition counteracts oxidative-nitrosative stress and poly(ADP-ribose) polymerase activation in tissue sites for diabetes complications. Diabetes 54:234–242PubMed PubMedCentral CrossRef
    Popova NK (2008) From gene to aggressive behavior: the role of brain serotonin. Neurosci Behav Physiol 38:471–475PubMed CrossRef
    Russell JW, Golovoy D, Vincent AM, Mahendru P, Olzmann JA, Mentzer A, Feldman EL (2002) High glucose-induced oxidative stress and mitochondrial dysfunction in neurons. FASEB J 16:1738–1748PubMed CrossRef
    Schmidt RE, Dorsey D, Parvin CA, Beaudet LN, Plurad SB, Roth KA (1997) Dystrophic axonal swellings develop as a function of age and diabetes in human dorsal root ganglia. J Neuropathol Exp Neurol 56:1028–1043PubMed CrossRef
    Scott CA, Rossiter JP, Andrew RD, Jackson AC (2008) Structural abnormalities in neurons are sufficient to explain the clinical disease and fatal outcome in experimental rabies in yellow fluorescent protein-expressing transgenic mice. J Virol 82:513–521PubMed PubMedCentral CrossRef
    Smart NL, Charlton KM (1992) The distribution of challenge virus standard rabies virus versus skunk street rabies virus in the brains of experimentally infected rabid skunks. Acta Neuropathol 84:501–508PubMed CrossRef
    Whitley RJ (2014) Herpes simplex virus. In: Scheld WM, Whitley RJ, Marra C (eds) Infections of the central nervous system, 4th edn. Lippincott Williams & Wilkins, Philadelphia, pp 137–156
    Yamamoto T, Ueki S (1977) Characteristics in aggressive behavior induced by midbrain raphe lesions in rats. Physiol Behav 19:105–110PubMed CrossRef
  • 作者单位:Alan C. Jackson (1) (2) (3)

    1. Department of Internal Medicine (Neurology), University of Manitoba, Winnipeg, Manitoba, Canada
    2. Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada
    3. Health Sciences Centre, GF-543, 820 Sherbrook Street, Winnipeg, Manitoba, R3A 1R9, Canada
  • 刊物主题:Neurosciences; Virology; Infectious Diseases; Immunology; Neurology;
  • 出版者:Springer US
  • ISSN:1538-2443
文摘
Rabies is an acute encephalomyelitis in humans and animals caused by rabies virus (RABV) infection. Because the neuropathological changes are very mild in rabies, it has been assumed that neuronal dysfunction likely explains the severe clinical disease. Recently, degenerative changes have been observed in neuronal processes (dendrites and axons) in experimental rabies. In vitro studies have shown evidence of oxidative stress that is caused by mitochondrial dysfunction. Recent work has shown that the RABV phosphoprotein (P) interacts with mitochondrial Complex I leading to overproduction of reactive oxygen species, which results in injury to axons. Amino acids at positions 139 to 172 of the P are critical in this process. Rabies vectors frequently show behavioral changes. Aggressive behavior with biting is important for transmission of the virus to new hosts at a time when virus is secreted in the saliva. Aggression is associated with low serotonergic activity in the brain. Charlton and coworkers performed studies in experimentally infected striped skunks with skunk rabies virus and observed aggressive behavioral responses. Heavy accumulation of RABV antigen was found in the midbrain raphe nuclei, indicating that impaired serotonin neurotransmission from the brainstem may account for the aggressive behavior. We now have an improved understanding of how RABV causes neuronal injury and how the infection results in behavioral changes that promote viral transmission to new hosts. Keywords Aggressive behavior Mitochondrial dysfunction Oxidative stress Pathogenesis Rabies Serotonin Viral encephalitis

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700