| pubmed-article:6315581 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6315581 | lifeskim:mentions | umls-concept:C0011849 | lld:lifeskim |
| pubmed-article:6315581 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
| pubmed-article:6315581 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:6315581 | lifeskim:mentions | umls-concept:C0597177 | lld:lifeskim |
| pubmed-article:6315581 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:6315581 | pubmed:dateCreated | 1984-1-7 | lld:pubmed |
| pubmed-article:6315581 | pubmed:abstractText | The B (nondiabetogenic) and D (diabetogenic) variants of encephalomyocarditis (EMC) virus were studied to further define the role of the interferon (IFN) system in murine virus-induced diabetes mellitus. The relationship between the initial multiplicity of infection with EMC-B and the IFN yield showed that cells infected with one IFN-inducing particle produce a maximum amount of IFN, whereas IFN production is suppressed in cells infected with two or more particles. The IFN yield induced by EMC-D was less than 5% of that induced by EMC-B, allowing the designation of the B and D variants as Ifp+ and Ifp-, respectively. The Ifp+ property of the virion was shown to be responsible for the greater sensitivity of EMC-B to exogenous IFN as a result of primed local IFN induction. The data indicate that different Ifp phenotypes occur in nature and are associated with the development of diabetes in mice. | lld:pubmed |
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| pubmed-article:6315581 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6315581 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6315581 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:6315581 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6315581 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:6315581 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:6315581 | pubmed:author | pubmed-author:JordanG WGW | lld:pubmed |
| pubmed-article:6315581 | pubmed:author | pubmed-author:CohenS HSH | lld:pubmed |
| pubmed-article:6315581 | pubmed:author | pubmed-author:BoltonVV | lld:pubmed |
| pubmed-article:6315581 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6315581 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:6315581 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6315581 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6315581 | pubmed:pagination | 605-11 | lld:pubmed |
| pubmed-article:6315581 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:6315581 | pubmed:meshHeading | pubmed-meshheading:6315581-... | lld:pubmed |
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| pubmed-article:6315581 | pubmed:meshHeading | pubmed-meshheading:6315581-... | lld:pubmed |
| pubmed-article:6315581 | pubmed:year | 1983 | lld:pubmed |
| pubmed-article:6315581 | pubmed:articleTitle | Relationship of interferon-inducing particle phenotype to encephalomyocarditis virus-induced diabetes mellitus. | lld:pubmed |
| pubmed-article:6315581 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6315581 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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