Abstract
Numerous questions are left unanswered in this volume and provide most intriguing areas for further investigations. In spite of considerable progress, knowledge is far from satisfactory even in the field of acute neurological diseases for which a definite direct etiology is well established. For some of these diseases, Japanese encephalitis for example, we are in great need of efficient vaccines.1 In addition, for such diseases it is especially urgent to develop better diagnostic procedures, since in even the most modern diagnostic virology facilities the etiologic agent remains unrecognized in over 30% of presumed cases of acute viral meningitis and in over 80% of presumed cases of acute viral encephalitis. Indeed, the precise etiologic diagnosis of viral infection of the nervous system (NS) in general is still fraught with difficulties. For example, the association of cerebral malformations and other neurological birth defects with antecedent viral infection of the mother is often beyond present methodologies.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Brandt, W. E.,1990, Development of dengue and Japanese encephalitis vaccines, J. Infect. Dis. 162: 577–583.
Berger, J. R., Sheremata, A., Resnick, L., Atherton, S., Fletcher, M. A., and Norenberg, M., 1989, Multiple sclerosis-like illness occurring with human immunodeficiency virus infection, Neurology 39: 324–329.
Trapp, B. D., Small, J. A., and Scangos, G. A., 1988, Dysmyelination in transgenic mice containing the early region of JC virus, in: Virus Infection and the Developing Nervous System ( R. T. Johnson and G. Lyon, eds.), Kluwer, Dordrecht, pp. 21–35.
Hinrichs, S. H., Nerenberg, M., Reynolds, R. K., Khoury, G., and Jay, G., 1987, A transgenic mouse model for human neurofibromatosis, Science 237: 1340–1343.
Lustig, S., Jackson, A. C., Hahn, C. S., Griffin, D. E., Strauss, E. G., and Strauss, J. H., 1988, Molecular basis of Sindbis virus neurovirulence in mice, J. Virol. 62: 2329–2336.
Evans, D. M. A., Dunn, G., Minor, P. D., Schild, G. C., Cann, A. J., Stanway, G., Almond, J. W, Currey, K., and Maizel, W, Jr., 1985, Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovirus genome, Nature 314: 548–550.
La Monica, N., Almond, J. W, and Racaniello, V. R., 1987, A mouse model for poliovirus neurovirulence identifies mutations that attenuate the virus for humans, J. Virol. 61: 2917–2920.
Duke, G. M., Osorio, J. E., and Palmenberg, A. C., 1990, Attenuation of Mengo virus through genetic engineering of the 5’ noncoding poly(C) tract, Nature 343: 474–476.
Calendoff, M. A., Faaberg, K. S., and Lipton, H. L., 1990, Genomic regions of neuro-virulence and attenuation in Theiler’s murine encephalomyelitis virus, Proc. Natl. Acad. Sci. U.S.A. 87: 978–982.
Contag, C. H., and Plagemann, P. G. W, 1989, Age-dependent poliomyelitis in mice: Expression of endogenous retrovirus correlates with cytocidal replication of lactate dehydrogenase-elevating virus in motor neurons, J. Virol. 63: 4362–4369.
Tada, H., Rappaport, J., Lashgari, M., Amini, S., Wong-Staal, E, and Khalili, K., 1990, Trans-activation of the JC virus late promoter by the tat protein of type 1 human immunodeficiency virus in glial cells, Proc. Natl. Acad. Sci. U.S.A. 87: 3479–3483.
Anomasiri, W. T., Tovell, D. R., and Tyrell, D. L. J., 1990, Paramyxovirus membrane protein enhances antibody production to new antigenic determinants in the actin molecule: A model for virus-induced autoimmunity, j Virol. 64: 3174–3184.
Galileo, D. S., Gray, G. E., Owens, G. C., Majors, J., and Sanes, J. R., 1990, Neurons and glia arise from a common progenitor in chicken optic tectum: Demonstration with two retro-viruses and cell type-specific antibodies, Proc. Natl. Acad. Sci. U.S.A. 87: 458–462.
Geller, A. I., and Freese, A., 1990, Infection of cultured central nervous system neurons with a defective herpes simplex virus 1 vector results in stable expression of Escherichia coli betagalactosidase, Proc. Natl. Acad. Sci. U.S.A. 87: 1149–1153.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1992 Plenum Press, New York
About this chapter
Cite this chapter
Specter, S., Bendinelli, M., Friedman, H. (1992). Continuing the Investigation. In: Specter, S., Bendinelli, M., Friedman, H. (eds) Neuropathogenic Viruses and Immunity. Infectious Agents and Pathogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5886-2_17
Download citation
DOI: https://doi.org/10.1007/978-1-4684-5886-2_17
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-5888-6
Online ISBN: 978-1-4684-5886-2
eBook Packages: Springer Book Archive