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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1996-1-16
|
| pubmed:abstractText |
Persistent viruses use several mechanisms to evade the immune response, including the generation of mutations that affect TCR recognition. It has recently been reported that spontaneous mutations at TCR contact sites within individual viral epitopes in certain persistent human viruses can abrogate or antagonize the recognition of the corresponding wild-type epitope, and it has been suggested that such mutations may contribute to viral persistence.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0952-7915
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
7
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
524-31
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading | |
| pubmed:year |
1995
|
| pubmed:articleTitle |
Viral mutations, TCR antagonism and escape from the immune response.
|
| pubmed:affiliation |
Scripps Research Institute, Department of Molecular and Experimental Medicine, La Jolla, California 92037, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
|