Ultrastructure of cranial nerves of rats inoculated with rabies virus

Minguetti, Guilberto; Hofmeister, R.; Hayashi, Yasuyoshi; Montano, J.A

doi:10.1590/s0004-282x1997000500002

Cited by 10 publications

(11 citation statements)

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“…Wallerian degeneration refers to a process that results when part of the axon degenerates in isolation of changes in the neuronal cell body. Minguetti and colleagues reported axonal degeneration and demyelination in both peripheral and cranial nerves of rodents inoculated with RV (181,182). Examination of mouse sciatic nerves inoculated with RV revealed that axonal degeneration mainly occurred in myelinated axons (183).…”

Section: Axonal Damage and Degenerationmentioning

confidence: 99%

Virus-induced neuronal dysfunction and degeneration

2009

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In general, virus infections of the brain are rather rare in the immune competent host. However, neurotropic viruses have developed mechanisms to exploit weaknesses in immunological defense mechanisms that eventually allow them to reach and infect CNS neurons. Once in the CNS, these viruses can induce significant neuronal dysfunction and degeneration of specific neuronal populations, sometimes leading to devastating, life-threatening consequences for the host. Here, we examine viruses with the ability to infect neurons and their resulting pathologies, their modes of entry to the CNS, and the cellular and molecular alterations that these viruses induce in neuronal cells. We also discuss the importance of various pathogenic events associated with viral infection of neurons and elaborate on the implications of recent findings suggesting that neuronal cells affected by viruses undergo a "dying back" pattern of degeneration. Finally, findings of virus-induced alterations in kinase activity are discussed in the context of recent evidence linking abnormalities in kinase signaling to the pathogenesis of major human neurodegenerative conditions.

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Section: Axonal Damage and Degenerationmentioning

confidence: 99%

Virus-induced neuronal dysfunction and degeneration

2009

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“…Although axonal transport of virus can lead to axonal degeneration [53], neuronal infection and axonal transport of virus may not result in axonal injury. A recombinant virus vector has been shown to be axonally transported in neurons without tissue damage [13].…”

Section: Axonal Pathology In Virus Infectionmentioning

confidence: 99%

Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination

Tsunoda

Fujinami

2002

Springer Semin Immunopathol

140

132

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The primary target in multiple sclerosis (MS) is believed to be either myelin itself (myelinopathy) or the myelin-forming cell, the oligodendrocyte (oligodendrogliopathy). Although axonal injury occurs in MS, it is regarded as a secondary event to the myelin damage. Here, the lesion develops from myelin (outside) to the axon (inside) (Outside-In model). Recently, gray matter lesions and axonal injury in normal-appearing white matter have also been reported in MS. This raises two questions. 1) Is axonal injury exclusively secondary to myelin damage or from a direct insult to the axon or neurons (axonopathy)? (2) Is the injured axon regarded as only an end result of pathology or disease, or can axonal injury contribute to the spread of secondary damage, including demyelination? The former is raised from the fact that axonal damage has been reported in several virus infections, including human immunodeficiency virus, human T-lymphotropic virus 1, herpes simplex virus and coronavirus, which also cause demyelination. The latter possibility where axonal injury leads to other changes is raised from the rather unexpected similarity between spinal cord injury (SCI) and MS where axonal injury, oligodendrocyte apoptosis and demyelination are all present. In SCI, transection of axons leads to delayed oligodendrocyte apoptosis with secondary demyelination. Neurofilament immunostaining of spinal cord sections demonstrates that axonal injury with oligodendrocyte apoptosis also precedes demyelination in an animal model for MS, Theiler's murine encephalomyelitis virus infection. This implies that axonal injury could trigger demyelination. In this instance, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model).

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“…Different virus families (Herpesviridae, Rhabdoviridae, Flaviviridae, Bornaviridae and Picornaviridae) include important human neurotropic viruses, such as herpes simplex virus, rabies virus, West Nile virus, poliovirus and others [8]. Neurotropic viruses often cause apoptosis of neurons [7,9,10] and axonal degeneration [11], which results in death of hosts or permanent neurological deficits [12]. For example, both poliovirus and West Nile virus have been shown to cause apoptosis of neurons [9,13,14] and axonal degeneration [15,16] in the CNS.…”

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confidence: 99%

Axonal Degeneration as a Self-Destructive Defense Mechanism Against Neurotropic Virus Infection

Tsunoda

2008

Future Virol.

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Theiler's murine encephalomyelitis virus (TMEV) and other neurotropic virus infections result in degeneration of each component of the neuron: apoptosis of the cell body, axonal (Wallerian) degeneration, and dendritic and synaptic pathology. In general, axonal degeneration is detrimental for hosts. However, axonal degeneration can be beneficial in the case of infection with neurotropic viruses that spread in the CNS using axonal transport. C57BL/Wld(S) (Wld(S), Wallerian degeneration slow mutant) mice are protected from axonal degeneration. Wld(S) mice infected with the neurovirulent GDVII strain of TMEV are more resistant to virus infection than wild-type mice, suggesting that axonal preservation contributes to the resistance. By contrast, infection with the less virulent Daniels strain of TMEV results in high levels of virus propagation in the CNS, suggesting that prolonged survival of axons in Wld(S) mice favors virus spread. Thus, axonal degeneration might be a beneficial self-destruct mechanism that limits the spread of neurotropic viruses, in the case of less virulent virus infection. We hypothesize that neurons use 'built-in' self-destruct protection machinery (compartmental neurodegeneration) against neurotropic virus infection, since the CNS is an immunologically privileged site. Early induction of apoptosis in the neuronal cell body limits virus replication. Wallerian degeneration of the axon prevents axonal transport of virus. Dendritic and synaptic degeneration blocks virus transmission at synapses. Thus, the balance between neurodegeneration and virus propagation may be taken into account in the future design of neuroprotective therapy.

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Ultrastructure of cranial nerves of rats inoculated with rabies virus

Cited by 10 publications

References 11 publications

Virus-induced neuronal dysfunction and degeneration

Virus-induced neuronal dysfunction and degeneration

Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination

Axonal Degeneration as a Self-Destructive Defense Mechanism Against Neurotropic Virus Infection

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