Ultrastructural and virological aspects of Langat virus-induced SSPE in suckling hamsters

David Walker, Y. Akov, B. G. Cain

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The morphology of subacute sclerosing panencephalitis (SSPE) lesions in hamsters following i.p. inoculation of Langat virus was studied by light microscopy and electron microscopy. The lesions' temporal relationship to virus presence and antibody production was studied by immunofluorescence, virus isolation from brains and brain cell cultures, and by antibody assay of serum and spinal fluid. All 10-day-old hamsters infected with Langat virus developed SSPE lesions, most prominently in the cerebellum, without any overt signs. The lesions appeared 10 days after infection, progressed in severity until Day 21 and persisted unaltered at least 3 months. They consisted of neuronal degeneration, calcification, and intracellular lipid accumulation. Virus was isolated from Days 3 to 15 and disappeared on Day 21. Demonstration by cerebellar immunofluorescence of viral antigen was observed 10 days after inoculation. Antibody appeared in the serum on Day 6, rose to very high titers by Day 21, and thereafter declined. Cell-associated virus was not demonstrable in negative brain-cell cultures. These findings suggest that SSPE in hamsters, associated with Langat virus infection, is biologically different from measles SSPE. Purkinje-cell lipid accumulation and mineralization sparing mitochondria were manifestations of the response of neurons to cell injury at the threshold of irreversibility.

Original languageEnglish (US)
Pages (from-to)604-612
Number of pages9
JournalBritish Journal of Experimental Pathology
Volume60
Issue number6
StatePublished - 1979
Externally publishedYes

Fingerprint

Tick-Borne Encephalitis Viruses
Subacute Sclerosing Panencephalitis
Cricetinae
Viruses
Fluorescent Antibody Technique
Brain
Cell Culture Techniques
Satellite Viruses
Lipids
Viral Antigens
Antibodies
Purkinje Cells
Measles
Virus Diseases
Serum
Cerebellum
Antibody Formation
Microscopy
Electron Microscopy
Mitochondria

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Ultrastructural and virological aspects of Langat virus-induced SSPE in suckling hamsters. / Walker, David; Akov, Y.; Cain, B. G.

In: British Journal of Experimental Pathology, Vol. 60, No. 6, 1979, p. 604-612.

Research output: Contribution to journalArticle

@article{592dc1604edf45c3a89e9247af01e991,
title = "Ultrastructural and virological aspects of Langat virus-induced SSPE in suckling hamsters",
abstract = "The morphology of subacute sclerosing panencephalitis (SSPE) lesions in hamsters following i.p. inoculation of Langat virus was studied by light microscopy and electron microscopy. The lesions' temporal relationship to virus presence and antibody production was studied by immunofluorescence, virus isolation from brains and brain cell cultures, and by antibody assay of serum and spinal fluid. All 10-day-old hamsters infected with Langat virus developed SSPE lesions, most prominently in the cerebellum, without any overt signs. The lesions appeared 10 days after infection, progressed in severity until Day 21 and persisted unaltered at least 3 months. They consisted of neuronal degeneration, calcification, and intracellular lipid accumulation. Virus was isolated from Days 3 to 15 and disappeared on Day 21. Demonstration by cerebellar immunofluorescence of viral antigen was observed 10 days after inoculation. Antibody appeared in the serum on Day 6, rose to very high titers by Day 21, and thereafter declined. Cell-associated virus was not demonstrable in negative brain-cell cultures. These findings suggest that SSPE in hamsters, associated with Langat virus infection, is biologically different from measles SSPE. Purkinje-cell lipid accumulation and mineralization sparing mitochondria were manifestations of the response of neurons to cell injury at the threshold of irreversibility.",
author = "David Walker and Y. Akov and Cain, {B. G.}",
year = "1979",
language = "English (US)",
volume = "60",
pages = "604--612",
journal = "International Journal of Experimental Pathology",
issn = "0959-9673",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Ultrastructural and virological aspects of Langat virus-induced SSPE in suckling hamsters

AU - Walker, David

AU - Akov, Y.

AU - Cain, B. G.

PY - 1979

Y1 - 1979

N2 - The morphology of subacute sclerosing panencephalitis (SSPE) lesions in hamsters following i.p. inoculation of Langat virus was studied by light microscopy and electron microscopy. The lesions' temporal relationship to virus presence and antibody production was studied by immunofluorescence, virus isolation from brains and brain cell cultures, and by antibody assay of serum and spinal fluid. All 10-day-old hamsters infected with Langat virus developed SSPE lesions, most prominently in the cerebellum, without any overt signs. The lesions appeared 10 days after infection, progressed in severity until Day 21 and persisted unaltered at least 3 months. They consisted of neuronal degeneration, calcification, and intracellular lipid accumulation. Virus was isolated from Days 3 to 15 and disappeared on Day 21. Demonstration by cerebellar immunofluorescence of viral antigen was observed 10 days after inoculation. Antibody appeared in the serum on Day 6, rose to very high titers by Day 21, and thereafter declined. Cell-associated virus was not demonstrable in negative brain-cell cultures. These findings suggest that SSPE in hamsters, associated with Langat virus infection, is biologically different from measles SSPE. Purkinje-cell lipid accumulation and mineralization sparing mitochondria were manifestations of the response of neurons to cell injury at the threshold of irreversibility.

AB - The morphology of subacute sclerosing panencephalitis (SSPE) lesions in hamsters following i.p. inoculation of Langat virus was studied by light microscopy and electron microscopy. The lesions' temporal relationship to virus presence and antibody production was studied by immunofluorescence, virus isolation from brains and brain cell cultures, and by antibody assay of serum and spinal fluid. All 10-day-old hamsters infected with Langat virus developed SSPE lesions, most prominently in the cerebellum, without any overt signs. The lesions appeared 10 days after infection, progressed in severity until Day 21 and persisted unaltered at least 3 months. They consisted of neuronal degeneration, calcification, and intracellular lipid accumulation. Virus was isolated from Days 3 to 15 and disappeared on Day 21. Demonstration by cerebellar immunofluorescence of viral antigen was observed 10 days after inoculation. Antibody appeared in the serum on Day 6, rose to very high titers by Day 21, and thereafter declined. Cell-associated virus was not demonstrable in negative brain-cell cultures. These findings suggest that SSPE in hamsters, associated with Langat virus infection, is biologically different from measles SSPE. Purkinje-cell lipid accumulation and mineralization sparing mitochondria were manifestations of the response of neurons to cell injury at the threshold of irreversibility.

UR - http://www.scopus.com/inward/record.url?scp=0018723757&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018723757&partnerID=8YFLogxK

M3 - Article

VL - 60

SP - 604

EP - 612

JO - International Journal of Experimental Pathology

JF - International Journal of Experimental Pathology

SN - 0959-9673

IS - 6

ER -