An ultrastructure study of cerebellar lesions induced in mice by three inoculations of avirulent Semliki Forest virus

Chew-Lim, May; Scott, T.; Webb, H. E.

doi:10.1007/bf00689557

Cited by 9 publications

(3 citation statements)

References 17 publications

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“…These authors concluded that demyelination in A 774-SFV infection probably results from direct viral activity rather than from an immunological reaction. Ultrastructural studies of mice infected with A774-SFV showed no changes in oligo-dendr0cytes (Chew-Lira et al 1978;Suckling et al 1978). It seemed unlikely, therefore, that direct viral damage to the oligodendrocyte was a cause of the demyelinative plaque.…”

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Demyelination in mice resulting from infection with a mutant of Semliki Forest virus

Sheahan¹,

Barrett

Atkins

1981

Acta Neuropathol

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Twelve of 34 weanling mice (35%) developed lesions in the brain and spinal cord following i.p. infection with 10(2) p.f.u. of a mutant of Semliki Forest virus (SFV). Six of 12 mice examined 13 days post infection (p.i.) showed meningo-encephalomyelitis with focal spongiform lesions in the grey and white matter. The spongiform lesions were characterised by necrosis of putative oligodendrocytes, myelinic vacuolation and mononuclear cell infiltration. Only one of six mice examined 21 days p.i. and one of six mice examined 28 days p.i. showed lesions which comprised reactive and dystrophic changes in the white matter. Spongiform lesions and pycnotic nuclei were not seen at these times. Viral nucleocapsids were seen in the early stages of the disease in putative necrotic oligodendrocytes. Mature virus particles were not seen. This was in contrast to mice infected with virulent wild-type SFV when lesions were more severe and were accompanied by large numbers of immature and mature virus particles. It is suggested that the demyelination in mice infected with mutant SFV results primarily from selective destruction of oligodendrocytes by the mutant virus.

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Demyelination in mice resulting from infection with a mutant of Semliki Forest virus

Sheahan¹,

Barrett

Atkins

1981

Acta Neuropathol

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“…This and previous studies [12,25,26,32,34] have attempted to conceptually link the consequences of a non-persistent virus infection by avirulent SFV with EAE. It has also been shown that multiple intraperitoneal injections of avirulent SFV can enhance demyelination [11], and infection of EAE-susceptible mice with avirulent SFV has been shown to facilitate EAE and render EAE-resistant mice susceptible [12,26]. Double intranasal infections of SJL mice by avirulent SFV can each lead to demyelination in the olfactory tract [32].…”

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confidence: 99%

Long‐term effects of Semliki Forest virus infection in the mouse central nervous system

Donnelly

Sheahan

Atkins

1997

Neuropathology Appl Neurobio

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Semliki Forest virus (SFV) infection of mice is used as a model to study pathogenic processes occurring in viral encephalitis and demyelinating disease. In this study, the long-term effects of infection by the avirulent M9 mutant of SPV on the central nervous system (CNS) of BALB/c and SJL mice were determined. The presence of infectious virus, viral RNA and cytokine mRNA in the brains of individual mice and the presence of lesions in the spinal cords of the same mice up to 360 days post-infection (d.p.i.) were analysed in order to detect any correlation between these parameters of pathogenesis. Infectious virus could not be detected beyond 7 d.p.i. for either mouse strain. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the presence of the E2 and nsP1 regions of the virus genome and mRNA for interferon-gamma and tumour necrosis factor-alpha. Viral RNA could be detected up to 90 d.p.i. for both mouse strains. Cytokine mRNA could be detected up to 28 d.p.i. for BALB/c mice but up to 360 d.p.i. for SJL mice. Inflammatory lesions, which were associated with cytokine mRNA expression, were not detected in BALB/c mice beyond 28 d.p.i. but were detected in two SJL mice at 90 d.p.i. It is concluded that M9-SFV infection induces long-term prolonged expression of pro-inflammatory cytokines in the CNS of the majority of SJL (but not BALB/c) mice which is not associated with persistence of the virus genome. M9-SFV infection of SJL mice may be a relevant model for the pathogenesis of multiple sclerosis in man.

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“…Primary damage to oligodendrocytes has been suggested by Sheahan, Barrett & Atkins (1980) who used a mutant strain of SFV. On the other hand, Chew-Lim, Scott & Webb (1978) using two or three intraperitoneal (i.p.) inoculations of SFV were unable to detect oligodendrocyte damage from infection by their strain of virus and other studies with this system clearly implicate an immune response in the pathogenesis of the CNS lesions (Jagelman et al., 1978).…”

Section: Introductionmentioning

confidence: 99%

Demyelination Induced in Mice by Avirulent Semliki Forest Virus. Ii. An Ultrastructural Study of Focal Demyelination in the Brain

Kelly

Blakemore

Jagelman³

et al. 1982

Neuropathology Appl Neurobio

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Four-week-old mice were infected intraperitoneally with an avirulent strain A7(74) of Semliki Forest virus (SFV) and killed at 4, 10, 15, 21 and 29 days after inoculation. Focal demyelinating lesions were present by 10 days. These were usually accompanied by a mononuclear infiltrate which included lymphocytes possessing characteristic cytoplasmic projections. These latter extended deep into the cytoplasm of adjacent cells, which were usually astrocytes and macrophages. Other features of the focal lesions were expansion of the extracellular space and demyelination which appeared to be fragmentation or lysis rather than stripping of myelin by macrophages. Although healing occurred in some mice after 4 weeks, acute lesions were still found in others of the same age. It was concluded that the demyelination probably had an immunological basis, and interaction between elements of the immune system and glial cells was a factor which inhibited orderly remyelination of the relatively mild lesions resulting from this infection.

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An ultrastructure study of cerebellar lesions induced in mice by three inoculations of avirulent Semliki Forest virus

Cited by 9 publications

References 17 publications

Demyelination in mice resulting from infection with a mutant of Semliki Forest virus

Demyelination in mice resulting from infection with a mutant of Semliki Forest virus

Long‐term effects of Semliki Forest virus infection in the mouse central nervous system

Demyelination Induced in Mice by Avirulent Semliki Forest Virus. Ii. An Ultrastructural Study of Focal Demyelination in the Brain

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