Coronavirus induced primary demyelination: indications for the involvement of a humoral immune response
Identifieur interne : 001B93 ( Main/Exploration ); précédent : 001B92; suivant : 001B94Coronavirus induced primary demyelination: indications for the involvement of a humoral immune response
Auteurs : F. Zimprich [Autriche] ; J. Winter [Allemagne] ; H. Wege [Allemagne] ; H. Lassmann [Autriche]Source :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 1991-12.
Abstract
Coronavirus MHV‐JHM infection of rodents can result in demyelinating encephalomyelitis. We analysed histological changes induced by coronavirus MHV‐JHM infection in Lewis rats. Besides an acute disease (AE), chronic panencephalitis (CPE) and subacute demyelinating encephalomyelitis (SDE) were induced. These disease types were differentiated by the incubation period, the localization of lesions, the type of tissue damage and distribution of virus antigen. In AE and CPE, virus antigen was detected in neurons, astrocytes and oligodendrocytes, whereas in SDE neurons lacked virus antigen. Viral nucleocapsid protein (N) was present in the cytoplasm and the spike protein (S) was displayed on the surface of infected neural cells. However, expression of S protein relative to N protein was severely impaired in SDE lesions. Quantitative analysis of infiltrating inflammatory cells revealed that the number of macrophages and T cells were similar in lesions of AE, CPE and SDE. In contrast to that, SDE lesions contained a significantly higher number of IgG† B cells and plasma cells. In addition active demyelinating SDE lesions displayed an enhanced IgG content and deposits of complement C9. These results indicate that virus induced primary demyelination could be a consequence of antibody mediated cytotoxicity. Furthermore, a reduction in the number of cells producing spike protein in the chronic forms of the disease indicates down‐regulation of this protein, possibly mediated by anti‐S antibodies.
Url:
DOI: 10.1111/j.1365-2990.1991.tb00750.x
Affiliations:
- Allemagne, Autriche
- Bavière, District de Basse-Franconie, Vienne (Autriche)
- Vienne (Autriche), Wurtzbourg
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Lassmann</name><affiliation wicri:level="3"><country xml:lang="fr">Autriche</country><wicri:regionArea>*Research Unit for Experiment Neuropathology, Austrian Academy of Sciences, Vienna</wicri:regionArea><placeName><settlement type="city">Vienne (Autriche)</settlement><region nuts="2" type="province">Vienne (Autriche)</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Autriche</country><wicri:regionArea>‡Neurological Institute, University of Vienna, Vienna</wicri:regionArea><placeName><settlement type="city">Vienne (Autriche)</settlement><region nuts="2" type="province">Vienne (Autriche)</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Autriche</country><wicri:regionArea>Correspondence address: Research Unit for Experimental Neuropathology, Austrian Academy of Sciences, Neurological Institute, Schwarzspanierstr. 17, A‐1090, Vienna</wicri:regionArea><placeName><settlement type="city">Vienne (Autriche)</settlement><region nuts="2" type="province">Vienne (Autriche)</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Neuropathology and Applied Neurobiology</title><title level="j" type="alt">NEUROPATHOLOGY APPLIED NEUROBIOLOGY</title><idno type="ISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><imprint><biblScope unit="vol">17</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="469">469</biblScope><biblScope unit="page" to="484">484</biblScope><biblScope unit="page-count">16</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1991-12">1991-12</date></imprint><idno type="ISSN">0305-1846</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1846</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronavirus MHV‐JHM infection of rodents can result in demyelinating encephalomyelitis. We analysed histological changes induced by coronavirus MHV‐JHM infection in Lewis rats. Besides an acute disease (AE), chronic panencephalitis (CPE) and subacute demyelinating encephalomyelitis (SDE) were induced. These disease types were differentiated by the incubation period, the localization of lesions, the type of tissue damage and distribution of virus antigen. In AE and CPE, virus antigen was detected in neurons, astrocytes and oligodendrocytes, whereas in SDE neurons lacked virus antigen. Viral nucleocapsid protein (N) was present in the cytoplasm and the spike protein (S) was displayed on the surface of infected neural cells. However, expression of S protein relative to N protein was severely impaired in SDE lesions. Quantitative analysis of infiltrating inflammatory cells revealed that the number of macrophages and T cells were similar in lesions of AE, CPE and SDE. In contrast to that, SDE lesions contained a significantly higher number of IgG† B cells and plasma cells. In addition active demyelinating SDE lesions displayed an enhanced IgG content and deposits of complement C9. These results indicate that virus induced primary demyelination could be a consequence of antibody mediated cytotoxicity. Furthermore, a reduction in the number of cells producing spike protein in the chronic forms of the disease indicates down‐regulation of this protein, possibly mediated by anti‐S antibodies.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Autriche</li></country><region><li>Bavière</li><li>District de Basse-Franconie</li><li>Vienne (Autriche)</li></region><settlement><li>Vienne (Autriche)</li><li>Wurtzbourg</li></settlement></list><tree><country name="Autriche"><region name="Vienne (Autriche)"><name sortKey="Zimprich, F" sort="Zimprich, F" uniqKey="Zimprich F" first="F." last="Zimprich">F. Zimprich</name></region><name sortKey="Lassmann, H" sort="Lassmann, H" uniqKey="Lassmann H" first="H." last="Lassmann">H. Lassmann</name><name sortKey="Lassmann, H" sort="Lassmann, H" uniqKey="Lassmann H" first="H." last="Lassmann">H. Lassmann</name><name sortKey="Lassmann, H" sort="Lassmann, H" uniqKey="Lassmann H" first="H." last="Lassmann">H. Lassmann</name></country><country name="Allemagne"><region name="Bavière"><name sortKey="Winter, J" sort="Winter, J" uniqKey="Winter J" first="J." last="Winter">J. Winter</name></region><name sortKey="Wege, H" sort="Wege, H" uniqKey="Wege H" first="H." last="Wege">H. Wege</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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