Hydrocephalus as a sequela of experimental myxovirus infections

Johnson, Richard T.; Johnson, Kenneth P.

doi:10.1016/0014-4800(69)90049-5

Cited by 108 publications

(33 citation statements)

References 20 publications

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“…Certainly, a better understanding of the precise mechanism(s) by which mumps virus leads to hydrocephalus will ultimately be required for a better appreciation of the role of virus-infected subventricular neurons in hydrocephalus development. To date, the preponderance of data suggests that hydrocephalus is the result of accumulation of virus-infected cell debris in the aqueduct of Sylvius, blocking cerebrospinal fluid egress (27,28,49). A similar mechanism is believed to be responsible for mumps virus hydrocephalus in humans (21,41,55).…”

Section: Discussionmentioning

confidence: 99%

Changes in Mumps Virus Gene Sequence Associated with Variability in Neurovirulent Phenotype

Rubin

Amexis

Pletnikov

et al. 2003

J Virol

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Mumps virus is highly neurotropic and, prior to widespread vaccination programs, was the major cause of viral meningitis in the United States. Nonetheless, the genetic basis of mumps virus neurotropism and neurovirulence was until recently not understood, largely due to the lack of an animal model. Here, nonneurovirulent (Jeryl Lynn vaccine) and highly neurovirulent (88-1961 wild type) mumps virus strains were passaged in human neural cells or in chicken fibroblast cells with the goal of neuroadapting or neuroattenuating the viruses, respectively. When tested in our rat neurovirulence assay against the respective parental strains, a Jeryl Lynn virus variant with an enhanced propensity for replication (neurotropism) and damage (neurovirulence) in the brain and an 88-1961 wild-type virus variant with decreased neurotropic and neurovirulent properties were recovered. To determine the molecular basis for the observed differences in neurovirulence and neuroattenuation, the complete genomes of the parental strains and their variants were fully sequenced. A comparison at the nucleotide level associated three amino acid changes with enhanced neurovirulence of the neuroadapted vaccine strain: one each in the nucleoprotein, matrix protein, and polymerase and three amino acid changes with reduced neurovirulence of the neuroattenuated wild-type strain: one each in the fusion protein, hemagglutinin-neuraminidase protein, and polymerase. The potential role of these amino acid changes in neurotropism, neurovirulence, and neuroattenuation is discussed.Mumps virus is a 15.3-kb enveloped, nonsegmented, negative-strand RNA virus in the Paramyxoviridae family. The mumps virus genome organization is 3Ј NP-P-M-F-SH-HN-L 5Ј, in which the abbreviations represent the genes encoding the following proteins: NP, nucleoprotein; P, phosphoprotein; M, matrix protein; F, fusion protein; SH, small hydrophobic protein; HN, hemagglutinin-neuraminidase protein; and L, polymerase (16). The virus causes mumps, an acute communicable viral disease typical of childhood. Mumps virus is transmitted through oropharyngeal secretions, with primary virus replication in the respiratory mucosa. Following the development of viremia, mumps virus infects a number of targets, including the central nervous system (CNS), and was a common cause of viral meningitis in the prevaccine era (6). The most common neurological manifestation of CNS infection is aseptic meningitis (23, 37). More rarely, clinical manifestations involve encephalitis (31, 38), cerebellar ataxia (12), and transverse myelitis and poliomyelitis-like disease (29,33). While symptoms are typically transient, CNS infection can produce significant morbidity (in such manifestations as, e.g., deafness [20,36,57]) and mortality, particularly in the case of encephalitis (38). Despite the clinical significance of mumps virus and the widespread international use of a number of mumps virus vaccines, little is known about the genetic basis for mumps virus attenuation or virulence.In this study, we sought to iden...

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Section: Discussionmentioning

confidence: 99%

Changes in Mumps Virus Gene Sequence Associated with Variability in Neurovirulent Phenotype

Rubin

Amexis

Pletnikov

et al. 2003

J Virol

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“…The lesions in one of the fetuses taken at 28 days were similar to those seen in the principal fetuses taken at 7 days. In the other control fetus from the same gilt, the lung was of normal size but had 5 Lung from principal fetus taken 7 days after virus inoculation. Severe epithelial destruction has resulted in obliteration of bronchial buds (short arrows).…”

Section: Resultsmentioning

confidence: 98%

Porcine Fetuses with Pulmonary Hypoplasia Resulting from Experimental Swine Influenza Virus Infection

et al. 1980

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Abstract. Porcine fetuses between 51 and 57 days of gestation were inoculated intraallantoically with swine influenza virus and examined 3,7, 13, 28 and 58 days after inoculation. At 3 and 7 days, severe epithelial necrosis was seen in most bronchial buds and there was moderate epithelial necrosis in more fully differentiated major bronchi. As a result of the epithelial injury, bronchial buds did not develop further and the surrounding mesoderm failed to differentiate. By 28 days, the lungs of inoculated fetuses were about one-half the size of the normal control lungs. Microscopically, the lungs of the inoculated fetuses were composed of major bronchi surrounded by multiple islands of cartilage, medium to large arteries and a few small, incompletely developed lobules. Influenza virus was isolated most consistently and in greatest quantity from the lung, trachea and chorion of inoculated fetuses. Influenza viral antigen was shown in the epithelium of bronchial buds, bronchi and the trachea by direct fluorescent antibody staining. Hemagglutination inhibiting antibodies to influenza virus were first found in the serum of an inoculated fetus at 13 days and in the sera of all inoculated fetuses at 28 and 58 days.

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“…Studies with common respiratory pathogens of myxoviruses and paramyxoviruses have revealed that they cause acute inflammation of the ependyma and meninges with various degrees of parenchymal involvement when viruses are inoculated into the brain of suckling rodents (5,13,19) . Hydrocephalus has developed in some suckling rodents as a sequela of intracerebral inoculation of such viruses (5,13,19) .…”

Section: Discussionmentioning

confidence: 99%

“…Hydrocephalus has developed in some suckling rodents as a sequela of intracerebral inoculation of such viruses (5,13,19) . Besides hydrocephalus as a late effect of infection of these viruses in the brain of suckling rodents, virus antigens were reported to persist in the brain of suckling mice inoculated intracerebrally with Sendai virus, one of the paramyxoviruses, for as long as 4 months (19) .…”

Section: Discussionmentioning

confidence: 99%

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Shimokata

1978

Microbiology and Immunology

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The pathogenicity of parainfluenza type 2 (croup-associated) virus known to cause infections of the respiratory tract in the early life of man was studied in the brain of mice. One-to 4-day-old sucklings and 4-week-old mice were inoculated intracerebrally with the virus. The virus multiplied in sucklings, but not in adults. Most mice inoculated intracerebrally with the virus appeared healthy. Histological examination showed minimum inflammatory changes, although moderate hydrocephalus developed in three of twenty-one sucklings by 6 weeks post-infection. Immunofluorescent study in sucklings showed viral antigens in ependymal lining cells and choroid plexus epithelium during the first two weeks, and parenchymal cells for more than two months. Virus specific antibody response was observed in adults, but not in sucklings. One interesting finding was that viral antigens persisted in six out of 11 suckling brains for one to two months.

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Hydrocephalus as a sequela of experimental myxovirus infections

Abstract: An immunological and histoimmunological study of gastric sulphoglycoproteins in healthy and aspirin-treated dogs I.

Cited by 108 publications

References 20 publications

Changes in Mumps Virus Gene Sequence Associated with Variability in Neurovirulent Phenotype

Changes in Mumps Virus Gene Sequence Associated with Variability in Neurovirulent Phenotype

Porcine Fetuses with Pulmonary Hypoplasia Resulting from Experimental Swine Influenza Virus Infection

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

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