Cerebellar Ataxia in Hamsters Inoculated with Rat Virus

Kilham, Lawrence; Margolis, George

doi:10.1126/science.143.3610.1047

Cited by 56 publications

(14 citation statements)

References 7 publications

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“…At that time, however, it was believed to be of genetic rather than of infectious origin. In the mid-sixties of this century it was reproduced experimentally by Kilham and co-workers [80,[86][87][88] in felines as well as in rodents and ferrets. Accord-ing to these studies, cerebellar ataxia is evidently the result of selective destruction of dividing cells in the outer germinal layer of a differentiating cerebellum.…”

Section: Parvoviruses As Pathogensmentioning

confidence: 99%

Parvoviruses: agents of distinct pathogenic and molecular potential

Siegl

Tratschin

1987

FEMS Microbiology Letters

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Parvoviruses are small, spherical and extremely stable particles with a genome of linear single‐stranded DNA. They are widespread in nature and thus have been in virtually every animal species and in man. Many parvoviruses were initially isolated by chance and could not be associated with clinical disease. Today, however, a considerable number of these agents are known to cause a broad spectrum of syndromes including fetal death, malformations, dwarfism, cerebellar hypolasia and ataxia, enteritis, panleukopenia, aplastic anemia, and immunologic disorders. Biological, pathological, and molecular studies revealed that all these syndromes are explainable on the basis of two predominant requirements for productive cytolytic parvovirus replication: the availability of cellular helper function(s) provided exclusively by mitotically active cells in the phase of cellular DNA replication, and by apparently specific, yet so far undefined cellular functions

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Section: Parvoviruses As Pathogensmentioning

confidence: 99%

Parvoviruses: agents of distinct pathogenic and molecular potential

Siegl

Tratschin

1987

FEMS Microbiology Letters

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“…Three serotypes (I-III) have been identified (13). Reovirus (14,15). The presence of a segmented genome has made it possible to isolate a number of recombinant clones containing different genome segments derived from either type I or type III reovirus (16).…”

mentioning

confidence: 99%

Generation of cytolytic T lymphocytes after reovirus infection: role of S1 gene.

Finberg¹,

Weiner²,

Fields³

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

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“…Neurological descriptions of the motor disturbances in Weaver mutants resemble those found in other 'agranular cerebellar' syndromes, such as that produced by viral infection [Kilham and Margolis, 1964], In general, the agranular symptoms are more severe than those found in the PCD mut ants. Closer comparison of these syn dromes might desirable as extracerebellar defects may differ.…”

Section: Neurological Signs and Substratesmentioning

confidence: 64%

Cerebellar Afferents in Normal and Weaver Mutant Mice

Grover¹,

Grüsser‐Cornehls²

1986

Brain Behav Evol

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Cerebellar afferents in 3-week-old normal and homozygous Weaver mutant mice were investigated using retrograde transport of horseradish peroxidase. Almost all afferents found in other mammals were demonstrated in both normal and mutant mice of this age. Labelling in the trigeminal nuclei in both mutants and normals was found only in cases in which the ansoparamedian or uvular lobules were included in the injection site, indicating that the projection domains of mossy fiber afferent systems retain their normal boundaries in the mutants despite a lack of normal synaptic partners. Thus the neurological signs which the Weaver exhibits from about the 10th postnatal day are unlikely to depend on primary or seondary losses of cerebellar afferents or on a breakdown of the gross topographic organization of these afferents.

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Cerebellar Ataxia in Hamsters Inoculated with Rat Virus

Cited by 56 publications

References 7 publications

Parvoviruses: agents of distinct pathogenic and molecular potential

Parvoviruses: agents of distinct pathogenic and molecular potential

Generation of cytolytic T lymphocytes after reovirus infection: role of S1 gene.

Cerebellar Afferents in Normal and Weaver Mutant Mice

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