Source:http://linkedlifedata.com/resource/pubmed/id/12533716
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
Pt 1
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pubmed:dateCreated |
2003-1-20
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pubmed:abstractText |
Inactivated influenza A virus and fixed, virus-infected cells induce type 1 interferon (IFN-alpha/beta) production in murine splenocytes. In this study, we have explored the nature of the virus-spleen cell interaction that leads to IFN-alpha/beta induction and the reason for the poor response to some virus strains. IFN-alpha/beta induction by horse serum-sensitive, but not -resistant, strains of influenza virus was inhibited in the presence of horse serum, indicating that binding of the virus to sialylated cell receptors is a necessary step in the induction process. Furthermore, influenza viruses A/PR/8/34 (H1N1) and A/WS/33 (H1N1), which were poor inducers of IFN-alpha/beta in spleen cells, were shown to have a more active neuraminidase than strains that induced higher IFN levels, and IFN-alpha/beta induction by A/PR/8/34 (H1N1) and A/WS/33 (H1N1) was restored in the presence of a neuraminidase inhibitor. Growth of virus in different cell types altered the level of IFN-alpha/beta induced in spleen cells by particular virus strains, suggesting that the nature of the carbohydrate moieties on the viral glycoproteins may also influence IFN-alpha/beta induction in this system. Consistent with this notion, treatment of egg-grown virus with periodate to oxidize viral carbohydrate greatly reduced its capacity for IFN-alpha/beta induction. Furthermore, induction of IFN-alpha/beta was inhibited in the presence of the saccharides yeast mannan and laminarin. Together these findings indicate: (i) a requirement for interaction of the virus with sialylated receptors on the IFN-producing cell; (ii) an influence of viral carbohydrate on the response; and (iii) possible involvement of a lectin-like receptor on the IFN-producing cell in the induction of IFN-alpha/beta or in regulation of this response.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1317
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
193-202
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12533716-Animals,
pubmed-meshheading:12533716-Cell Line,
pubmed-meshheading:12533716-Cells, Cultured,
pubmed-meshheading:12533716-Glycosylation,
pubmed-meshheading:12533716-Humans,
pubmed-meshheading:12533716-Influenza A virus,
pubmed-meshheading:12533716-Interferon Type I,
pubmed-meshheading:12533716-Macrophages, Peritoneal,
pubmed-meshheading:12533716-Mice,
pubmed-meshheading:12533716-N-Acetylneuraminic Acid,
pubmed-meshheading:12533716-Neuraminidase,
pubmed-meshheading:12533716-Species Specificity,
pubmed-meshheading:12533716-Spleen
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pubmed:year |
2003
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pubmed:articleTitle |
Virus-cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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