| pubmed-article:10908662 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10908662 | lifeskim:mentions | umls-concept:C0019761 | lld:lifeskim |
| pubmed-article:10908662 | lifeskim:mentions | umls-concept:C0149678 | lld:lifeskim |
| pubmed-article:10908662 | lifeskim:mentions | umls-concept:C0443288 | lld:lifeskim |
| pubmed-article:10908662 | pubmed:issue | 16 | lld:pubmed |
| pubmed-article:10908662 | pubmed:dateCreated | 2000-9-5 | lld:pubmed |
| pubmed-article:10908662 | pubmed:abstractText | Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that causes infectious mononucleosis and is etiologically associated with malignancies of multiple origins. EBV enters cells through a cascade of interactions between its envelope glycoprotein gp350 and the gp42-gH-gL complex with cellular receptors. Membrane fusion is catalyzed by the binding of gp42, a member of the C type lectin family, to HLA class II molecule HLA-DR, -DP, or -DQ. Here we demonstrate that only a subset of HLA-DQ alleles mediates EBV entry, indicating that individuals expressing these alleles may offer unique sites for EBV infection and subsequent sequelae. Additionally, the specific site within HLA-DQ determined to be essential for EBV entry is homologous to a site within MHC class I shown by structural studies to bind to the C type-lectin-like natural killer receptor, providing insight into the biochemical nature of the gp42-HLA class II interaction. | lld:pubmed |
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| pubmed-article:10908662 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10908662 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10908662 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10908662 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10908662 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:10908662 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10908662 | pubmed:author | pubmed-author:LongneckerRR | lld:pubmed |
| pubmed-article:10908662 | pubmed:author | pubmed-author:HaanK MKM | lld:pubmed |
| pubmed-article:10908662 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10908662 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:10908662 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10908662 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10908662 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10908662 | pubmed:pagination | 9252-7 | lld:pubmed |
| pubmed-article:10908662 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10908662 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10908662 | pubmed:articleTitle | Coreceptor restriction within the HLA-DQ locus for Epstein-Barr virus infection. | lld:pubmed |
| pubmed-article:10908662 | pubmed:affiliation | Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611, USA. | lld:pubmed |
| pubmed-article:10908662 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10908662 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10908662 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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