Pathogenicity of mumps virus in the marmoset

Saika, Shizuko; Kidokoro, Minoru; Ohkawa, Tokitada; Aoki, Atuko; Suzuki, Kota

doi:10.1002/jmv.2119

Cited by 15 publications

(12 citation statements)

References 15 publications

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“…Consistent with this hematogenous route of CNS invasion, infected cells are usually first detected in the choroid plexus and in close association with cerebral blood vessels (34,39). Once inside the CSF, the viruses may invade the different membranes surrounding the CNS, the ependyma, and the superficial lining of the cerebral cortex (34,49), followed by infection of neurons and glia cells in close proximity and subsequent spread into deeper layers (19,26,29). Taken together, these observations suggest that paramyxoviruses use classical hematogenous CNS invasion pathways described for several other neurotropic viruses (17,33).…”

Section: Discussionmentioning

confidence: 78%

“…This provides ample opportunity for infected lymphocytes to traffic through the blood-brain and blood-choroid plexus barrier and locally release virus, starting infection of resident epithelial and endothelial cells (12,15). Consistent with this hematogenous route of CNS invasion, infected cells are usually first detected in the choroid plexus and in close association with cerebral blood vessels (34,39). Once inside the CSF, the viruses may invade the different membranes surrounding the CNS, the ependyma, and the superficial lining of the cerebral cortex (34,49), followed by infection of neurons and glia cells in close proximity and subsequent spread into deeper layers (19,26,29).…”

Section: Discussionmentioning

confidence: 97%

“…This study shows remarkable parallels between CDV entry into the CNS of ferrets and the mechanisms of brain invasion by other Paramyxoviridae. Several paramyxoviruses with neurovirulent potential, including morbilliviruses, mumps virus, and Newcastle disease virus, efficiently infect circulating lymphocytes, resulting in a cell-associated viremia that lasts throughout the symptomatic disease phase (32,34,50). This provides ample opportunity for infected lymphocytes to traffic through the blood-brain and blood-choroid plexus barrier and locally release virus, starting infection of resident epithelial and endothelial cells (12,15).…”

Section: Discussionmentioning

confidence: 99%

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Canine Distemper Virus Uses both the Anterograde and the Hematogenous Pathway for Neuroinvasion

Rudd

Cattaneo

Messling

2006

J Virol

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Canine distemper virus (CDV), a member of the Morbillivirus genus that also includes measles virus, frequently causes neurologic complications, but the routes and timing of CDV invasion of the central nervous system (CNS) are poorly understood. To characterize these events, we cloned and sequenced the genome of a neurovirulent CDV (strain A75/17) and produced an infectious cDNA that expresses the green fluorescent protein. This virus fully retained its virulence in ferrets: the course and signs of disease were equivalent to those of the parental isolate. We observed CNS invasion through two distinct pathways: anterogradely via the olfactory nerve and hematogenously through the choroid plexus and cerebral blood vessels. CNS invasion only occurred after massive infection of the lymphatic system and spread to the epithelial cells throughout the body. While at early time points, mostly immune and endothelial cells were infected, the virus later spread to glial cells and neurons. Together, the results suggest similarities in the timing, target cells, and CNS invasion routes of CDV, members of the Morbillivirus genus, and even other neurovirulent paramyxoviruses like Nipah and mumps viruses.Canine distemper virus (CDV) and the closely related viruses that infect marine mammals have the highest incidence of central nervous system (CNS) complications among viruses of the genus Morbillivirus. Up to 30% of dogs exhibit signs of neurologic involvement during or after CDV infection, and most wild carnivores that succumb to CDV have some evidence of CNS infection (8,18,20,38,51). With 1 in 1,000 cases, the neurovirulent potential of measles virus (MV) is comparatively lower, but CNS complications remain one of the main problems associated with MV infections in countries with an established health care system (32). Because of its relatively high degree of neurovirulence and the availability of a sensitive small animal model, CDV is an ideal candidate to characterize the events involved in morbillivirus neuroinvasion.All morbilliviruses display a strong lymphotropism, which correlates with the presence of their principal receptor, the signaling lymphocytic activation molecule (SLAM, CD150), on a variety of immune cells (6,36,40). In ferrets infected with a virulent CDV strain, more than 50% of circulating peripheral blood mononuclear cells (PBMC) contain infectious virus, and up to 10% of PBMC in MV-infected monkeys are virus positive (46, 53). Because of these findings and the fact that morbilliviruses are highly cell associated, it is thought that the contact between virus and CNS occurs through infected PBMC. Previous studies of typical wild-type isolates like strain A75/17 in dogs further support this theory (38).At the onset of the symptomatic disease around 14 days after intranasal inoculation, infected cells are predominantly detected in the perivascular spaces of the CNS, the choroid plexus, and the ependyma (19,39). Around 3 weeks after infection, CDV-positive glial cells and neurons are found in the white matter, and...

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Canine Distemper Virus Uses both the Anterograde and the Hematogenous Pathway for Neuroinvasion

Rudd

Cattaneo

Messling

2006

J Virol

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“…Mongolian MuVs belong to genotype H, and all originated from the hospitalized mumps patients. Meanwhile, reliable animal models using common marmosets or neonatal rats to evaluate the neurovirulence of MuV have been proposed (24)(25)(26)(27). Therefore, we assessed the neurovirulence of the Mongolian isolate, MuVi-MNG09-024, in a rat model (Fig.…”

Section: Mumps Epidemics In Mongoliamentioning

confidence: 99%

Characterization of Mumps Viruses Circulating in Mongolia: Identification of a Novel Cluster of Genotype H

et al. 2011

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Although mumps virus is still causing annual epidemics in Mongolia, very few epidemiological and virological data have been reported. We describe here the first phylogenetic analysis data on the mumps viruses circulated in Mongolia in 2009. We detected 21 mumps virus cDNAs and obtained a virus isolate from 32 throat swabs of mumps patients in Ulaanbaatar, the capital of Mongolia. The phylogenetic analyses based on the 316 nucleotides of the small hydrophobic gene show that these sequences form a single cluster, with the closest relatedness to the viruses belonging to genotype H. According to the recommendation of the World Health Organization, Mongolian mumps viruses could be classified into a novel genotype because the divergence between new sequences and genotype H reference viruses is >5% (6.3 to 8.2%). However, additional analyses based on the fusion gene, the hemagglutinin-neuraminidase gene, and the whole-genome indicate that the divergences between the Mongolian isolate and other genotype H strains never exceed the within-genotype divergences of other genotypes. These results suggest that Mongolia strains should be included in genotype H and that the current criteria for mumps virus genotyping should be revised. We propose here that the Mongolian viruses should be classified as a new subgenotype termed H3. Since previous epidemiological studies suggested that genotypes H may be associated with central nervous system diseases, we evaluated the neurovirulence of the Mongolian isolate in the neonatal rat system. However, the virus does not exhibit prominent neurovirulence in rats.

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“…10 Much of our current understanding of mumps virus pathogenesis is based on hamster and monkey models, but the unnatural routes of inoculation and the inability to distinguish attenuated mumps virus strains from wild-type strains makes the relevance of these findings questionable. 11,12 One study with marmosets shows that intravenous inoculation with a clinical mumps virus isolate induces meningitis, whereas another study in which rhesus macaques were infected via the natural route with a clinical mumps virus isolate shows that these animals develop parotitis but no fever or neurological symptoms. 10,12 Although these findings suggest that monkeys might be a candidate model for mumps virus pathogenesis studies, the costs and ethical considerations limit the applicability of this model for mumps.…”

mentioning

confidence: 99%