Rabies pathogenesis

Murphy, Frederick A.

doi:10.1007/bf01314774

Cited by 190 publications

(110 citation statements)

References 51 publications

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“…It is not known how the infection is transmitted over the synaptic cleft but the relative high density of virus-binding receptors in preparations of brain synaptosomes (Vahlne et al, 1978 makes release from the presynaptic nerve terminal and a postsynaptic adsorption possible. Such a course of events has been suggested for other virus infections of the CNS (Murphy, 1977;von Pottelsberghe et al, 1979). The present paper reports the first observations on how the neuron is infected by HSV via attachment and uptake of virus into neuronal processes.…”

Section: Discussionmentioning

confidence: 93%

Uptake and Transport of Herpes Simplex Virus in Neurites of Rat Dorsal Root Ganglia Cells in Culture

Lycke

Kristensson

Svennerholm

et al. 1984

Journal of General Virology

127

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SUMMARYAttachment and neuritic transport of herpes simplex virus (HSV) type 1 (McIntyre) were studied in a cell culture system with dissociated cells of rat dorsal root ganglia. The two-chamber cell culture system containing a diffusion barrier penetrated by neurites of cultured sensory neurons permitted infection of neurites extending outside the diffusion barrier without exposure of the neuronal cell soma. HSV adsorbed to neuritic extensions and reached the neuronal soma within 1.5 h post-inoculation. Neuritic uptake and transport of HSV were inhibited in the presence of cytochalasin B. Internalization of virus in neurites was preceded by attachment of virus to the neurite plasma membrane. Neurites transported viral nucleocapsids (NC) through the diffusion barrier of the cultures. Destruction of the neuritic extensions before or shortly after peripheral virus inoculation blocked spread of infection to the cell soma. No infection was established when neuritic extensions were exposed to viral NC and NC were then not observed inside the neurite plasma membrane. Virus produced in neurons, when HSV was inoculated into the inner culture chamber containing the neuronal cell bodies, was transported as enveloped virus in cytoplasmic vesicles from the neuronal cell body towards the periphery. Schwann cells were infected by viropexis. Shortly after infection virions were observed in vacuoles of the cytoplasm.

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Section: Discussionmentioning

confidence: 93%

Uptake and Transport of Herpes Simplex Virus in Neurites of Rat Dorsal Root Ganglia Cells in Culture

Lycke

Kristensson

Svennerholm

et al. 1984

Journal of General Virology

127

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“…In this respect, scrapie may resemble neurotropic viruses such as rabies (Murphy, 1977), herpes simplex (Wildy et al, 1982) and pseudorabies (Field & Hill, 1974). There is one study (with a different combination of scrapie strain and mouse genotype) showing intraneuronal transport of agent from eye to contralateral superior colliculus (Fraser, 1982), but otherwise nothing is known of which cells transport scrapie in nerves or in the CNS.…”

mentioning

confidence: 99%

Pathogenesis of Mouse Scrapie: Evidence for Spread of Infection from Central to Peripheral Nervous System

Kimberlin¹,

Field

Walker³

1983

Journal of General Virology

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“…Similar to other viral diseases, early reports suggested that apoptosis played an important role in causing cell death in animals inoculated with a laboratory-adapted CVS strain of rabies virus [101][102][103] Apoptosis was found only in suckling mice when intracerebrally inoculated with rabies virus (CVS strain), and correlated with viral load and severity of clinical symptoms progressing to death, but apoptosis was absent in adult mice and in peripherally inoculated animals [104][105][106][107][108]. More neurovirulent strains produced less apoptosis and vice versa [107,109].…”

Section: Bat Rabiesmentioning

confidence: 98%

Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

et al. 2016

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Rabies viral encephalitis, though one of the oldest recognized infectious disease of humans, remains an incurable, fatal encephalomyelitis, despite advances in understanding of its pathobiology. Advances in science have led us on the trail of the virus in the host, but the sanctuaries in which the virus remains hidden for its survival are unknown. Insights into host-pathogen interactions have facilitated evolving immunologic therapeutic strategies, though we are far from a cure. Most of the present-day knowledge has evolved from in vitro studies using fixed (attenuated) laboratory strains that may not be applicable in the clinical setting. Much remains to be unraveled about this elusive virus. This review attempts to re-examine the current advances in understanding of the pathobiology of the rabies virus that modulate the diagnosis, treatment, and prevention of this fatal disease.

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Rabies pathogenesis

Cited by 190 publications

References 51 publications

Uptake and Transport of Herpes Simplex Virus in Neurites of Rat Dorsal Root Ganglia Cells in Culture

Uptake and Transport of Herpes Simplex Virus in Neurites of Rat Dorsal Root Ganglia Cells in Culture

Pathogenesis of Mouse Scrapie: Evidence for Spread of Infection from Central to Peripheral Nervous System

Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

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