Experimental rabies virus infection in Artibeus jamaicensis bats with CVS-24 variants (original) (raw)

Abstract

An experimental model of rabies was established in the fruit-eating bat species Artibeus jamaicensis. The infections caused by CVS-N2c and CVS-B2c, which are both stable variants of CVS-24, were compared after inoculation of adult bats in the right masseter muscle. CVS-N2c produced neurologic signs of rabies with paresis, ataxia, and inability to fly, while CVS-B2c did not produce neurologic signs. Bats were sacrificed and the distribution of rabies virus antigen was assessed in tissue sections with immunoperoxidase staining. Both viruses spread to the brain stem and bilaterally to the trigeminal ganglia by days 2 to 3. CVS-N2c had disseminated widely in the central nervous system (CNS) by day 4 and had involved the spinal cord, thalamus, cerebellum, and cerebral cortex. CVS-B2c had infected neurons in the spinal cord on day 5 and in the cerebellum, thalamus, and cerebral cortex on day 6. Infected pyramidal neurons of the hippocampus were observed on day 5 in CVS-N2c infection, but infected neurons were never noted in the hippocampus in CVS-B2c infection. CVS-N2c infected many more neurons and more prominently involved neuronal processes than CVS-B2c. CVS-N2c spread more efficiently in the CNS than CVS-B2C. Morphologic changes of apoptosis or biochemical evidence of DNA fragmentation were not observed in neurons with either virus after this route of inoculation. The different neurovirulent properties of these CVS variants in this model were not related to their in vivo ability to induce apoptosis.

Access this article

Log in via an institution

Subscribe and save

• Get 10 units per month
• Download Article/Chapter or eBook
• 1 Unit = 1 Article or 1 Chapter
• Cancel anytime Subscribe now

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

• Carbone KM, Duchala CS, Griffin JW, Kincaid AL, Narayan O (1987). Pathogenesis of Borna disease in rats: evidence that intra-axonal spread is the major route for virus dissemination and the determinant for disease incubation. J Virol 61: 3431–3440.
  CAS PubMed Google Scholar
• Domingo E, Escarmis C, Sevilla N, Moya A, Elena SF, Quer J, Novella IS, Holland JJ (1996). Basic concepts in RNA virus evolution. FASEB J 10: 859–864.
  CAS PubMed Google Scholar
• Feiden W, Kaiser E, Gerhard L, Dahme E, Gylstorff B, Wandeler A, Ehrensberger F (1988). Immunohistochemical staining of rabies virus antigen with monoclonal and polyclonal antibodies in paraffin tissue sections. Zentralbl Veterinarmed [_B_] 35: 247–255.
  CAS Google Scholar
• Galelli A, Baloul L, Lafon M (2000). Abortive rabies virus central nervous infection is controlled by T lymphocyte local recruitment and induction of apoptosis. J NeuroVirol 6: 359–372.
  Article CAS PubMed Google Scholar
• Jackson AC (1991). Biological basis of rabies virus neurovirulence in mice: comparative pathogenesis study using the immunoperoxidase technique. J Virol 65: 537–540.
  CAS PubMed Google Scholar
• Jackson AC (1994). Animal models of rabies virus neurovirulence. In: Current Topics in Microbiology and Immunology, Volume 187: Lyssaviruses. Rupprecht CE, Dietzschold B, Koprowski H (eds). Springer-Verlag: Berlin, pp 85–93.
  Google Scholar
• Jackson AC (1997). Rabies. In: Viral Pathogenesis. Nathanson N, Ahmed R, Gonzalez-Scarano F, Griffin DE, Holmes K, Murphy FA, Robinson HL (eds). Lippincott-Raven: Philadelphia, pp 575–591.
  Google Scholar
• Jackson AC (2000). Rabies. Can J Neurol Sci 27: 278–282.
  CAS PubMed Google Scholar
• Jackson AC, Park H (1998). Apoptotic cell death in experimental rabies in suckling mice. Acta Neuropathol 95: 159–164.
  Article CAS PubMed Google Scholar
• Jackson AC, Reimer DL (1989). Pathogenesis of experimental rabies in mice: an immunohistochemical study. Acta Neuropathol 78: 159–165.
  Article CAS PubMed Google Scholar
• Jackson AC, Rossiter JP (1997a). Apoptosis plays an important role in experimental rabies virus infection. J Virol 71: 5603–5607.
  CAS PubMed Google Scholar
• Jackson AC, Rossiter JP (1997b). Apoptotic cell death is an important cause of neuronal injury in experimental Venezuelan equine encephalitis virus infection of mice. Acta Neuropathol 93: 349–353.
  Article CAS PubMed Google Scholar
• Jackson AC, Ye H, Phelan CC, Ridaura-Sanz C, Zheng Q, Li Z, Wan X, Lopez-Corella E (1999). Extraneural organ involvement in human rabies. Lab Invest 79: 945–951.
  CAS PubMed Google Scholar
• Kohji T, Matsumoto Y (2000). Coexpression of Fas/FasL and Bax on brain and infiltrating T cells in the central nervous system is closely associated with apoptotic cell death during autoimmune encephalomyelitis. J Neuroimmunol 106: 165–171.
  Article CAS PubMed Google Scholar
• Morimoto K, Hooper DC, Carbaugh H, Fu ZF, Koprowski H, Dietzschold B (1998). Rabies virus quasispecies: implications for pathogenesis. Proc Natl Acad Sci USA 95: 3152–3156.
  Article CAS PubMed Google Scholar
• Morimoto K, Hooper DC, Spitsin S, Koprowski H, Dietzschold B (1999). Pathogenicity of different rabies virus variants inversely correlates with apoptosis and rabies virus glycoprotein expression in infected primary neuron cultures. J Virol 73: 510–518.
  CAS PubMed Google Scholar
• Noah DL, Drenzek CL, Smith JS, Krebs JW, Orciari L, Shaddock J, Sanderlin D, Whitfield S, Fekadu M, Olson JG, Rupprecht CE, Childs JE (1998). Epidemiology of human rabies in the United States, 1980 to 1996. Ann Intern Med 128: 922–930.
  CAS PubMed Google Scholar
• Ortega J, Castro-Arellano I (2001). Artibeus jamaicensis. Mammalian Species 662: 1–9.
  Article Google Scholar
• Price JL, Everard CO (1977). Rabies virus and antibody in bats in Grenada and Trinidad. J Wildl Dis 13: 131–134.
  CAS PubMed Google Scholar
• Ray SK, Schaecher KE, Shields DC, Hogan EL, Banik NL (2000). Combined TUNEL and double immunofluorescent labeling for detection of apoptotic mononuclear phagocytes in autoimmune demyelinating disease. Brain Res Brain Res Protoc 5: 305–311.
  Article CAS PubMed Google Scholar
• Theerasurakarn S, Ubol S (1998). Apoptosis induction in brain during the fixed strain of rabies virus infection correlateswith onset and severity of illness. J Neuro Virol 4: 407–414.
  CAS Google Scholar
• Ubol S, Kasisith J (2000). Reactivation of Nedd-2, a developmentally down-regulated apoptotic gene, in apoptosis induced by a street strain of rabies virus. J Med Microbiol 49: 1043–1046.
  CAS PubMed Google Scholar
• Varughese P (2000). Human rabies in Canada—1924–2000. Can Commun Dis Rep 26: 210–211.
  CAS PubMed Google Scholar

Download references

Author information

Authors and Affiliations

1. Departments of Medicine and Microbiology and Immunology, Queen’s University, Kingston, Ontario, Canada
   Jessica E. Reid & Alan C. Jackson
2. Kingston General Hospital, Connell 725, 76 Stuart Street, K7L 2V7, Kingston, Ontario, Canada
   Alan C. Jackson

Authors

1. Jessica E. Reid
   You can also search for this author inPubMed Google Scholar
2. Alan C. Jackson
   You can also search for this author inPubMed Google Scholar

Corresponding author

Correspondence toAlan C. Jackson.

Rights and permissions

About this article

Cite this article

Reid, J.E., Jackson, A.C. Experimental rabies virus infection in Artibeus jamaicensis bats with CVS-24 variants.Journal of NeuroVirology 7, 511–517 (2001). https://doi.org/10.1080/135502801753248097

Download citation

• Received: 17 January 2001
• Accepted: 22 June 2001
• Issue Date: November 2001
• DOI: https://doi.org/10.1080/135502801753248097

Keywords