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Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
On histology of brain tissue, infection typically appears as encephalitis with Negri bodies, which are eosinophilic neuronal cytoplasmic inclusions. Negri bodies are pathognomonic for rabies, but are not always present in tissue specimens.
Rabies and other lyssaviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Thiravat Hemachudha, Jiraporn Laothamatas, Henry Wilde
Active retrograde transneuronal transfer for each synaptic step (12 h interval) proceeds at high speed (not distance-dependent) (reviewed in detail [21]). Within 4 days of infection of the first motor neurons in the spinal cord, dorsal root ganglia in the same segment are heavily infected. Such transneuronal transfer affects the dorsal root ganglia of the whole spinal cord, brain stem, and corticospinal pathways resulting in infection of spinal motor neurons, interneurons, and higher-order CNS neurons. Negri bodies are a pathological hallmark of rabies. They result from excessive accumulation of RNP in the cytoplasm [6,8].
R
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Rabies [Latin: rabere, to rage] George Gottfried Zinke of Jena proposed that the saliva of the rabid dog was infectious in 1804. This remained unproved until 1879, when Victor Galtier (1846–1908) of Paris managed to produce a paralytic form of rabies in rabbits by inoculating them with infective material. Curare was used to relax the muscles in patients with rabies in 1838. Changes in the central nervous system were reported by Louis Pasteur (1822–1895) and colleagues in 1881, and the first inoculation with antirabies vaccine was performed by him on July 6 1885. Negri bodies, characteristic cell inclusions, were observed by Italian microbiologist, Adelchi Negri (1867–1912) in 1903, but he mistook them for parasitic protozoal organisms. See hydrophobia.
Modern biologics for rabies prophylaxis and the elimination of human cases mediated by dogs
Published in Expert Opinion on Biological Therapy, 2020
Terapong Tantawichien, Charles E. Rupprecht
Taxonomically, rabies is caused by highly neurotropic, rod-shaped, enveloped, single-stranded, negative-sense RNA viruses, within the Family Rhabdoviridae, Genus Lyssavirus (Figure 1). As with other genera within the family, lyssaviruses form a monophyletic clade, based upon phylogenetic analyses and all viral species have a similar morphology, genome, and replication strategy [5]. The inner, viral nucleoprotein (N) is tightly associated with RNA to form a helical capsid, containing anti-genomic RNA, generated during replication and serving as a template for synthesis of complexes with genomic RNA. During translation, the capped and polyadenylated mRNAs are transcribed from each gene (i.e., in the 3′ to 5′ direction). The five primary viral proteins have multiple structural and functional roles. The viral phosphoprotein (P) is an essential replication co-factor. The P protein interacts with the N protein. Both are associated with genomic RNA and the viral RNA-dependent RNA polymerase (L protein), to form a viral ribonucleoprotein (RNP) complex. Within neurons, the viral RNP, with an abundance of N protein, contributes to intracytoplasmic inclusions (i.e., Negri bodies). Negri bodies are of historical diagnostic importance, representative of compartmentalized viral replication and assembly [6]. In addition, the P protein is a primary interferon (IFN) antagonist, targeting IFN induction [7]. The matrix (M) protein maintains structural features between the inner and outer viral proteins. In addition, the M protein has a role in viral replication and assembly. Together with the P protein, the M protein is involved in the process of evading innate immune responses by regulation of cell signaling [8]. The outer glycoprotein (G) mediates attachment to host receptors (such as the neuronal cell adhesion molecule and p75NTR, among others) and fusion between viral and endosomal membranes, with viral genome release into the cytoplasm of the cell [9,10]. The detection of G protein by the host leads to the formation of virus-neutralizing antibodies (VNA), as the primary immune effector. Besides a primary role in RNA synthesis, the L protein is also involved in mRNA capping and transcriptional initiation [11].