Post-Exposure Local Treatment of Mice Infected with Rabies with Two Axonal Flow Inhibitors, Colchicine and Vinblastine

Bijlenga, G.; Heaney, Thomas

doi:10.1099/0022-1317-39-2-381

Cited by 36 publications

(17 citation statements)

References 1 publication

(1 reference statement)

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“…Motor nerve conduction studies were normal including F-wave latencies but showed reduced CMAP amplitudes in the right median and ulnar nerves compared to the left (5.52 mV vs. 10.89 mV and 4.76 mV vs. 9.6 mV in the median and ulnar nerves, respectively). H-reflexes to gastrocnemius -soleus were normal and symmetric.…”

Section: Patientmentioning

confidence: 94%

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Mitrabhakdi

Shuangshoti

Wannakrairot

et al. 2005

Journal of the Neurological Sciences

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Section: Patientmentioning

confidence: 94%

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Mitrabhakdi

Shuangshoti

Wannakrairot

et al. 2005

Journal of the Neurological Sciences

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“…This is a normal pathway of diffusion for other neurotropic viruses such as herpes simplex type 1 (Kristensson & Lycke, 1971), measles (Fournier et al, 1985) and rabies viruses (Murphy et al, 1973;Bijlenga & Heaney, 1978;Giliet et al, 1986) and seems probable for poliovirus. Our results show the presence of viral genomes in neuronal processes of poliovirus-infected monkeys.…”

Section: Discussionmentioning

confidence: 99%

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Couderc

Christodoulou

Kopecká

et al. 1989

Journal of General Virology

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SUMMARYUsing in situ hybridization techniques for viral RNA and employing a specific riboprobe, we have detected virus in neural cells of monkeys infected with poliovirus type l (PV-1) by the intraspinal route. In monkeys paralysed after inoculation of a neurovirulent revertant of PV-1/Sabin strain, viral RNA was detected in motor neurons and their processes, and in polymorphonuclear and small neural cells. Quantitative in situ hybridization provided evidence of viral replication in individual cells suggesting that the death of motor neurons was due to the direct effect of poliovirus replication in these cells. The histological study of neural lesions of monkeys paralysed after infection with the attenuated Sabin strain of PV-1 revealed two major differences compared to monkeys infected with a virulent strain: (i) the number of destroyed moto r neurons was reduced and limited to the site of inoculation and (ii) the inflammatory reaction was localized but more intense. An account is given of the difference in histopathology induced by virulent and attenuated strains of PV-1 in the central nervous system.

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“…Accordingly, the involvement of microtubules in the transport of PV was investigated. Vinblastine, known as an inhibitor of tubulin polymerization and used to inhibit axonal transport in vivo (7,11,42,45), was employed to treat the sciatic nerve to examine whether microtubules are involved in transport (Fig. 3A).…”

Section: Pv Endocytosis At Neuromuscular Junctions Of the Tg Mousementioning

confidence: 99%

Receptor (CD155)-Dependent Endocytosis of Poliovirus and Retrograde Axonal Transport of the Endosome

Ohka

Matsuda

Tohyama

et al. 2004

J Virol

113

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Poliovirus (PV), when injected intramuscularly into the calf, is incorporated into the sciatic nerve and causes an initial paralysis of the inoculated limb in transgenic mice carrying the human PV receptor (hPVR/CD155) gene. Here, we demonstrated by using an immunoelectron microscope that PV particles exist on vesicle structures in nerve terminals of neuromuscular junctions. We also demonstrated in glutathione S-transferase pulldown experiments that the dynein light chain, Tctex-1, interacts directly with the cytoplasmic domain of hPVR. In the axons of differentiated rat PC12 cells transfected with expression vectors for hPVRs, vesicles composed of PV and hPVR␣, as well as a mutant hPVR␣ (hPVRM␣) that had a reduced ability to bind Tctex-1, colocalized with Tctex-1. However, vesicles containing PV, dextran, and hPVR␣ had only retrograde motion, while those containing PV, dextran, and hPVRM␣ had anterograde or retrograde motion. Topical application of the antimicrotubule agent vinblastine to the sciatic nerve reduced the amount of virus transported from the calf to the spinal cord. These results suggest that direct efficient interaction between the cytoplasmic domain and Tctex-1 is essential for the efficient retrograde transport of PV-containing vesicles along microtubules in vivo.In humans, paralytic poliomyelitis is considered to result from an invasion by circulating poliovirus (PV) into the central nervous system, probably via the blood-brain barrier. The notion is supported by a previous study using a mouse model (44). In that study, it was demonstrated that circulating PV after intravenous inoculation appears to cross the blood-brain barrier at a high rate, and the neural dissemination pathway from the skeletal muscle is not the primary dissemination route of the circulating virus to the central nervous system. Along with this pathway of dissemination, a neural pathway has been reported in humans (32), monkeys (20), and PV-sensitive transgenic (Tg) mice carrying the human PV receptor (hPVR/ CD155) gene (35,36), and it appears to be important in causing provocation poliomyelitis (14). Using the Tg mouse line, we demonstrate that PV inoculated into the calf is incorporated into the sciatic nerve and retrogradely transported through the axons as intact virion particles, that one of the fast retrograde axonal transport systems is involved in viral dissemination, and that the pathogenesis of PV infection via the neural pathway is inhibited by the anti-hPVR monoclonal antibody (MAb) p286, which is able to block the infection (35).hPVR is a member of the immunoglobulin (Ig) superfamily, with three linked extracellular Ig-like domains followed by a membrane-spanning domain and a cytoplasmic domain (CP). Two membrane-bound forms (hPVR␣ and hPVR␦) and two secreted forms (hPVR␤ and hPVR␥) derived by alternative splicing are potentially expressed in human cells (28). Membrane-bound hPVRs are considered to play important roles in the early steps of infection, such as binding of the virus to the cell surface, penetration...

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Post-Exposure Local Treatment of Mice Infected with Rabies with Two Axonal Flow Inhibitors, Colchicine and Vinblastine

Cited by 36 publications

References 1 publication

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Difference in neuropathogenetic mechanisms in human furious and paralytic rabies

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Receptor (CD155)-Dependent Endocytosis of Poliovirus and Retrograde Axonal Transport of the Endosome

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