Abstract
Rabies virus produces an acute central nervous system infection in warmblooded animals and humans, causing an illness with overt clinical symptoms that are unlike any other disease. It is not entirely clear how the virus manages to invade the nervous system (both peripheral and central) although there is general agreement about the neural pathways used by the virus. Despite extensive efforts to research the pathogenesis of rabies using state-of-the-art methods of the times for more than a century, there is still much more that needs to be understood about the pathogenetic process of rabies virus. Recent investigations of molecular correlates of rabies pathogenesis have revealed that a significant determinant of viral pathogenicity resides in the glycoprotein of rabies virus. The critical amino acid arginine at position 333 of the glycoprotein sequence of 505 amino acids seems to be essential for the virus to exert its lethal effects on the infected host.
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Wunner, W.H., Koprowski, H. (1989). Clinical and Molecular Aspects of Rabies Virus Infections of the Nervous System. In: Gilden, D.H., Lipton, H.L. (eds) Clinical and Molecular Aspects of Neurotropic Virus Infection. Developments in Medical Virology, vol 5. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1675-6_10
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