Involvement of morbilliviruses in the pathogenesis of demyelinating disease

Sips, Gregorius J.; Chesik, Daniel; Glazenburg, Lisa; Wilschut, Jan; Keyser, Jacques De; Wilczak, Nadine

doi:10.1002/rmv.526

Cited by 31 publications

(45 citation statements)

References 216 publications

(303 reference statements)

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“…3,6,29 Similarly, in distemper or measles encephalitis, perivascular cuffings usually develop in the subacute stage of the disease, after the initial virus-induced lymphopenia subsides. 12,25 Alternatively, day-old chickens might have an immature immune system that does not allow severe lymphocytic inflammation, as is observed in mature birds. Edema of the neuroparenchyma was also observed in vNDV-infected birds and was characterized by multifocal to coalescing areas with swollen neurons and severe vacuolation of the neuropil and white matter.…”

Section: Discussionmentioning

confidence: 99%

Neuropathogenic Capacity of Lentogenic, Mesogenic, and Velogenic Newcastle Disease Virus Strains in Day-Old Chickens

et al. 2015

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Strains of Newcastle disease virus (NDV) have different abilities to elicit neurologic signs. To determine the capacity of different NDV strains to replicate and cause lesions in the brain, independently of their peripheral replication, 1-day-old chickens were inoculated in the subdural space with 7 NDV strains of different virulence (4 velogenic, 2 mesogenic, 1 lentogenic). Velogenic strains induced severe necrotizing and heterophilic ventriculitis and meningitis, as well as edema of the neuroparenchyma, and replicated extensively in the nervous tissue by day 2 postinfection, as demonstrated by immunohistochemistry, when all infected birds died. Clinical signs, microscopic lesions, and viral replication were delayed (days 3 and 4 postinfection) with mesogenic strains. Velogenic and mesogenic NDV strains replicated mainly in neurons, and immunolabeling was first detected in surface-oriented areas (periventricular and submeningeal), possibly as a reflection of the inoculation route. The lentogenic NDV strain did not cause death of infected birds; replication was confined to the epithelium of the ependyma and choroid plexuses; and lesions consisted of lymphoid aggregates limited to the choroid plexuses. Results show that extensive NDV replication in the brain is typical of velogenic and mesogenic, but not lentogenic, NDV strains. In addition, this study suggests that differences in the rate of NDV replication in nervous tissue, not differences in neurotropism, differentiate velogenic from mesogenic NDV strains. This study indicates that intracerebral inoculation might be used as an effective method to study the mechanisms of NDV neuropathogenesis.

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Section: Discussionmentioning

confidence: 99%

Neuropathogenic Capacity of Lentogenic, Mesogenic, and Velogenic Newcastle Disease Virus Strains in Day-Old Chickens

et al. 2015

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“…Evidence suggesting an infectious agent in the etiology of MS includes the association of multiple viral infections with MS [2] , the precedence of relapses by infection [3,4] and epidemiological studies demonstrating MS outbreaks in areas with no previous history of the disease, most notable in the Faroe Islands [5] . Additionally, human viral infections are known to cause demyelination both through direct lysis of oligodendrocytes, as occurs in progressive multifocal leukoencephalopathy brought on by polyoma JC virus infection, and indirectly, as is the case in post-infectious (PI) acute disseminated encephalomyelitis initiated by vaccination or infection [6] and subacute sclerosing panencephalitis caused by measles virus infection [7] . In addition, virus-induced demyelination is demonstrable in animals.…”

Section: Introductionmentioning

confidence: 99%

Restraint Stress Fails to Render C57BL/6 Mice Susceptible to Theiler’s Virus-Induced Demyelination

Steelman¹,

Alford²,

Young³

et al. 2009

Neuroimmunomodulation

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Objectives: Multiple sclerosis is a degenerative disease of the CNS with a pathology consistent with immunological mediation. Although its cause is unknown, multiple factors are thought to influence both the onset and exacerbation of the disease, including both genetic background as well as environmental factors. Methods: We are interested in the effect of psychological stress on the onset and exacerbation of Theiler’s virus-induced demyelinating disease (TVID), a murine model of MS in which viral persistence facilitates demyelination. In the current study, we determined whether chronic restraint stress (RS)-induced immunosuppression could result in the establishment of a persistent CNS infection in the normally TVID-resistant C57BL/6 mouse strain, resulting in demyelination. Results: Our data indicated that RS repeated over the course of 7 days was not sufficient to cause decreases in virus-specific adaptive immunity, and did not significantly alter CNS viral levels. Furthermore, chronic repeated RS lasting until 4 weeks after infection altered neither the development of virus-specific IgG nor motor function determined by Rotarod analysis. In addition, histological analysis of the CNS of stressed mice indicated no inflammation or demyelination on day 193 after infection. Conclusion: These results suggest that stress alone is not sufficient to overcome genetic resistance to TVID in the C57BL/6 mouse strain.

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“…All morbilliviruses have the potential to cause neurological complications with delayed onset (4,25). These manifestations are always associated with extensive infection of the CNS and are invariably fatal (27). In MeV infection, individuals with certain immune defects are at high risk of developing measles inclusion body encephalitis several weeks to months after they recover from the acute disease, while infection before the age of two years increases the possibility of subacute sclerosing panencephalitis occurring years to decades later (20,24).…”

Section: Discussionmentioning

confidence: 99%

Region between the Canine Distemper Virus M and F Genes Modulates Virulence by Controlling Fusion Protein Expression

Anderson

Messling

2008

J Virol

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Morbilliviruses, including measles and canine distemper virus (CDV), are nonsegmented, negative-stranded RNA viruses that cause severe diseases in humans and animals. The transcriptional units in their genomes are separated by untranslated regions (UTRs), which contain essential transcription and translation signals. Due to its increased length, the region between the matrix (M) protein and fusion (F) protein open reading frames is of particular interest. In measles virus, the entire F 5 region is untranslated, while several start codons are found in most other morbilliviruses, resulting in a long F protein signal peptide (Fsp). To characterize the role of this region in morbillivirus pathogenesis, we constructed recombinant CDVs, in which either the M-F UTR was replaced with that between the nucleocapsid (N) and phosphoprotein (P) genes, or 106 Fsp residues were deleted. The Fsp deletion alone had no effect in vitro and in vivo. In contrast, substitution of the UTR was associated with a slight increase in F gene and protein expression. Animals infected with this virus either recovered completely or experienced prolonged disease and death due to neuroinvasion. The combination of both changes resulted in a virus with strongly increased F gene and protein expression and complete attenuation. Taken together, our results provide evidence that the region between the morbillivirus M and F genes modulates virulence through transcriptional control of the F gene expression.

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Involvement of morbilliviruses in the pathogenesis of demyelinating disease

Cited by 31 publications

References 216 publications

Neuropathogenic Capacity of Lentogenic, Mesogenic, and Velogenic Newcastle Disease Virus Strains in Day-Old Chickens

Neuropathogenic Capacity of Lentogenic, Mesogenic, and Velogenic Newcastle Disease Virus Strains in Day-Old Chickens

Restraint Stress Fails to Render C57BL/6 Mice Susceptible to Theiler’s Virus-Induced Demyelination

Region between the Canine Distemper Virus M and F Genes Modulates Virulence by Controlling Fusion Protein Expression

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