Mouse Encephalitis Induced by Avirulent Semliki Forest Virus

Chew-Lim, May

doi:10.1177/0300985875012005-00605

Cited by 18 publications

(7 citation statements)

References 9 publications

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“…The titer of the virus is higher earlier in the brains of the 14-day-old mice than in adults studied previously [6]. Many more cells may become involved before there is control of viral spread by a competent immunological system that in the adult normally reacts t o limit the extent of necrotic lesions in the mousc central nervous system.…”

Section: Discussionmentioning

confidence: 83%

Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Chew-Lim

1978

Vet Pathol

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Abstract. Avirulent Semliki Forest Virus when inoculated intracerebrally and intraperitoneally into 14-day-old Swiss A,G mice induced a lethal encephalitis. There was destruction of neurones, especially pyramidal cells of the hippocampus, despite a rising serum antibody titer.Avirulent Semliki Forest Virus has been classified as an alphavirus of the Togaviridae [14]. This virus, given intraperitoneally to 3 to 4-week-old Swiss A2G mice, induced a non-lethal acute encephalitis that resolved by 6 weeks without any histological evidence of neuronal damage (61. Other workers have shown that mice up to 15 days old were infected lethally with 1 to 3 plaque forming units of the virus/LD,, by any strain of the virus administered by any route (21. Materials and MethodsThe Semliki Forst Virus was obtained from Dr. C. J . Bradish (Microbiological Research Establishment. Porton. Salisbury) and was the same avirulent strain as used previously 161. It had a titer of 1u7.s intracerebral mean lethal doses (ICLD,,,)/0.02 ml in suckling mice but was not lethal for mice 21 days old or older. The suckling mouse ICLD,,, was calculated by the method of Reed and Muench I 161. Dilutions of stock virus were made in sterile bovine albumin phosphate. p H 7.3. The intracerebral dose of 0.02 milliliters had a titer of 104.7 ICLD5, and 0.1 milliliter of the intraperitoneal dose was titered at 10"" ICLD,,.Ninety 2-week-old Swiss A,G mice wcre given the virus intracerebrally and 40 were given the virus intraperitoneally. The mice were of either sex from a statistically randomly bred colony maintained within a specific-pathogen-free barrier. Sick and paralysed mice were killed with anaesthetic ether and brains were sampled for histology on days 1-7, 11 and 14 after inoculation. At each sampling single half brains were taken for virus isolation. The assay of virus infectivity was by plaque counting in agar suspensions of primary chick embryo cells 121. One mouse was bled on days 4-7 for serum, which then was given the serum neutralisation-index test 11. 91. This index was the logarithm of antiserum dilution giving 50% reduction of virus plaques. An index greater than 2.5 protects mice against challenge with the virulent strain of the virus 121.Mouse brains for histology were fixed in 5% buffered formol-saline for at least 7 days. Whole brains were sectioned in the frontal plane into three parts. The anterior cut was in front of the hippocampus and the posterior cut at the junction of the midbrain and hind 393

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Section: Discussionmentioning

confidence: 83%

Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Chew-Lim

1978

Vet Pathol

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“…Histologically, avirulent SF virus infection produces at least four types of lesions; perivascular infiltration, microgliosis, astrocyte hypertrophy, and focal spongiform vacuolation (6,13,18,26). All the cell types involved in the lesions represent possible sources of increased lysosomal enzyme production.…”

Section: Resultsmentioning

confidence: 99%

Brain lysosomal glycosidase activity in immunosuppressed mice infected with avirulent Semliki forest virus

Suckling¹,

Jagelman²,

Webb³

1977

Infect Immun

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“…Peripheral infection with the A7 isolate of SFV results in demyelination in 25% of the mice, and inflammatory pathology (perivascular cuffing, meningeal inflammation, and microcystic foci) in 95% of the mice [149,150]. Perivascular cuffs are apparent at three days postinfection [79], and the acute encephalitis affecting both the brain and spinal cord, with focal lesions and perivascular cuffing of lymphocytes, resolves by six weeks postinfection [184,185]. Demyelination of the brain and spinal cord can be seen as early as day 10 postinfection, is maximal between 14 and 21 days postinfection, and is largely recovered (assessed via electron-microscopic autoradiography) in some mice (but not all) by 28-36 days postinfection [31,186,187].…”

Section: The Pathologymentioning

confidence: 99%

Viral mouse models used to study multiple sclerosis: past and present

Libbey

Fujinami

2021

Arch Virol

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Multiple sclerosis (MS) is a common inflammatory demyelinating disease of the central nervous system. Although the etiology of MS is unknown, genetics and environmental factors, such as infections, play a role. Viral infections of mice have been used as model systems to study this demyelinating disease of humans. Three viruses that have long been studied in this capacity are Theiler’s murine encephalomyelitis virus, mouse hepatitis virus, and Semliki Forest virus. This review describes the viruses themselves, the infection process, the disease caused by infection and its accompanying pathology, and the model systems and their usefulness in studying MS.

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Mouse Encephalitis Induced by Avirulent Semliki Forest Virus

Cited by 18 publications

References 9 publications

Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Brain lysosomal glycosidase activity in immunosuppressed mice infected with avirulent Semliki forest virus

Viral mouse models used to study multiple sclerosis: past and present

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