Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1992-2-20
|
| pubmed:abstractText |
Inbred mice with genetically determined severe combined immunodeficiency (SCID) lack mature T and B lymphocyte functions. To distinguish direct viral effects in the pathogenesis of myocarditis from those mediated by antigen-specific and histocompatibility-complex-restricted host immunity, we inoculated coxsackievirus B3 into homozygous young adult SCID mice. We found that infected SCID mice invariably developed extensive myocarditis between 7 and 14 days postinoculation with high subsequent mortality. Histopathologic examination of the infected SCID myocardium indicated multiple foci of cardiomyocyte necrosis and a delayed pleomorphic inflammatory infiltrate. Immunohistochemically, the coxsackievirus B3-infected SCID heart contained frequent clusters of macrophages (Mac-1+) as well as other cells that may represent nonspecific phagocytic or cytolytic effectors. In situ hybridization with radiolabeled cDNA probes for enteroviral genome indicated a significant excess of positive-strand genome in the SCID myocardium compared with that in similarly infected non-SCID controls, with hybridization signals localized primarily to cardiomyocytes. In vitro culture confirmed persistent viremia and a vast excess of infective virus in the SCID myocardium relative to infected non-SCID controls. Thus, direct viral mechanisms in the production of cardiomyocyte injury in coxsackievirus B3-infected mice appear to be more important than previously recognized, particularly in the setting of unrestricted viral proliferation.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0023-6837
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
66
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
24-31
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:1309927-Animals,
pubmed-meshheading:1309927-Antigens, Viral,
pubmed-meshheading:1309927-Cardiomyopathies,
pubmed-meshheading:1309927-Coxsackievirus Infections,
pubmed-meshheading:1309927-DNA, Viral,
pubmed-meshheading:1309927-Disease Models, Animal,
pubmed-meshheading:1309927-Enterovirus B, Human,
pubmed-meshheading:1309927-Enterovirus Infections,
pubmed-meshheading:1309927-Heart,
pubmed-meshheading:1309927-Immunohistochemistry,
pubmed-meshheading:1309927-Immunophenotyping,
pubmed-meshheading:1309927-Lymphocyte Depletion,
pubmed-meshheading:1309927-Macrophages,
pubmed-meshheading:1309927-Major Histocompatibility Complex,
pubmed-meshheading:1309927-Mice,
pubmed-meshheading:1309927-Mice, Inbred C3H,
pubmed-meshheading:1309927-Mice, SCID,
pubmed-meshheading:1309927-Myocarditis,
pubmed-meshheading:1309927-Myocardium,
pubmed-meshheading:1309927-Necrosis,
pubmed-meshheading:1309927-Nucleic Acid Hybridization,
pubmed-meshheading:1309927-Severe Combined Immunodeficiency,
pubmed-meshheading:1309927-Virus Replication
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Enteroviral infection of mice with severe combined immunodeficiency. Evidence for direct viral pathogenesis of myocardial injury.
|
| pubmed:affiliation |
John P. Robarts Research Institute, University of Western Ontario, London, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|