Subacute Sclerosing Panencephalitis: Experimental Infection in Primates

Albrecht, Paul; Burnstein, Theodore; Klutch, M J; Hicks, H. Mason; Ennis, F A

doi:10.1126/science.831255

Cited by 55 publications

(18 citation statements)

References 28 publications

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“…Alterna- tively, immunity induced by the HA antigen may be intrinsically poorer than immunity induced by the F antigen. Retarded neurological disease despite the prior presence of antibodies against the HA protein has been previously reported (17,19).…”

Section: Discussionmentioning

confidence: 95%

Protection of mice from fatal measles encephalitis by vaccination with vaccinia virus recombinants encoding either the hemagglutinin or the fusion protein.

Drillien

Spehner

Kirn

et al. 1988

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

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Vaccinia virus recombinants encoding the hemagglutinin or fusion protein of measles virus have been constructed. Infection of cell cultures with the recombinants led to the synthesis of authentic measles proteins as judged by their electrophoretic mobility, recognition by antibodies, glycosylation, proteolytic cleavage, and presentation on the cell surface. Mice vaccinated with a single dose of the recombinant encoding the hemagglutinin protein developed antibodies capable of both inhibiting hemagglutination activity and neutralizing measles virus, whereas animals vaccinated with the recombinant encoding the fusion protein developed measles neutralizing antibodies. Mice vaccinated with either of the recombinants resisted a normally lethal intracerebral inoculation of a cell-associated measles virus subacute sclerosing panencephalitis strain.

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Section: Discussionmentioning

confidence: 95%

Protection of mice from fatal measles encephalitis by vaccination with vaccinia virus recombinants encoding either the hemagglutinin or the fusion protein.

Drillien

Spehner

Kirn

et al. 1988

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

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“…In a transgenic line which expresses SLAM ubiquitously (60), infection of the central nervous system was examined, and this revealed that MV could induce an acute neurological syndrome in mice less than 3 weeks old. In contrast, SSPE strains show strong neurovirulence and can induce lethal neurological disease in immunocompetent, genetically unaltered animals (2,31,32,33,64,70). We previously reported that the SSPE Osaka-2 strain induced acute encephalopathy in 3-week-old hamsters several days after intracerebral inoculation (29).…”

Section: Measles Virus (Mv) Is the Causative Agent For Acute Measles mentioning

confidence: 99%

The F Gene of the Osaka-2 Strain of Measles Virus Derived from a Case of Subacute Sclerosing Panencephalitis Is a Major Determinant of Neurovirulence

Ayata

Takeuchi

Takeda

et al. 2010

J Virol

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Measles virus (MV) is the causative agent for acute measles and subacute sclerosing panencephalitis (SSPE). Although numerous mutations have been found in the MV genome of SSPE strains, the mutations responsible for the neurovirulence have not been determined. We previously reported that the SSPE Osaka-2 strain but not the wild-type strains of MV induced acute encephalopathy when they were inoculated intracerebrally into 3-week-old hamsters. The recombinant MV system was adapted for the current study to identify the gene(s) responsible for neurovirulence in our hamster model. Recombinant viruses that contained envelope-associated genes from the Osaka-2 strain were generated on the IC323 wild-type MV background. The recombinant virus containing the M gene alone did not induce neurological disease, whereas the H gene partially contributed to neurovirulence. In sharp contrast, the recombinant virus containing the F gene alone induced lethal encephalopathy. This phenotype was related to the ability of the F protein to induce syncytium formation in Vero cells. Further study indicated that a single T461I substitution in the F protein was sufficient to transform the nonneuropathogenic wild-type MV into a lethal virus for hamsters.

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“…However, histological lesions are mainly of neuronal degeneration and cellular infiltration in limited areas of CNS. In animals with immunity to MV at appropriate degrees, chronic encephalitis involving larger areas of CNS can be produced as shown in the hamsters, inoculated with the Niigata-1 strain (Katow et al, 1973), ferrets with D. R. strain (Thormar , Arnesen and Mehta, 1977) and rhesus monkeys with IP 3 strain (Albrecht et al ., 1977). These results indicate an importance of immune status of the hosts in the course of virus-induced encephalitis.…”

Section: 3mentioning

confidence: 99%

Comparative Aspects of Pathogenicity of Measles, Canine Distemper, and Rinderpest Viruses

Yamanouchi¹

1980

JJMSB

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Subacute Sclerosing Panencephalitis: Experimental Infection in Primates

Cited by 55 publications

References 28 publications

Protection of mice from fatal measles encephalitis by vaccination with vaccinia virus recombinants encoding either the hemagglutinin or the fusion protein.

Protection of mice from fatal measles encephalitis by vaccination with vaccinia virus recombinants encoding either the hemagglutinin or the fusion protein.

The F Gene of the Osaka-2 Strain of Measles Virus Derived from a Case of Subacute Sclerosing Panencephalitis Is a Major Determinant of Neurovirulence

Comparative Aspects of Pathogenicity of Measles, Canine Distemper, and Rinderpest Viruses

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