pubmed-article:1840619 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0024267 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0003451 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0521026 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0039195 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0017968 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0546816 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C1853126 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C1953353 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0205171 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
pubmed-article:1840619 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:1840619 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:1840619 | pubmed:dateCreated | 1991-4-17 | lld:pubmed |
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pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:abstractText | Isolates of lymphocytic choriomeningitis virus (LCMV) that elicit a cytotoxic T-lymphocyte response (CTL+) have been compared with isolates that suppress the CTL response (CTL-) in an effort to map this phenotype. A single amino acid change in the glycoprotein of the LCMV Armstrong (ARM) strain is consistently associated with the CTL- trait and the ability of the virus to persist (P+). The CTL+ P- parental strain spontaneously gives rise to CTL- P+ variants within lymphoid tissues of mice persistently infected from birth. To map the structural basis of the phenotype, the complete RNA sequence of LCMV ARM 53b (CTL+) was compared with that of its variant ARM clone 13 (CTL-). Differences in 5 of 10,600 nucleotides were found. Three changes are noted in the large L RNA segment, and two are noted in the small S RNA segment. Only two of the changes distinguishing CTL+ from CTL- isolates affect amino acid coding: lysine to glutamine at amino acid 1079 of the polymerase protein, and phenylalanine to leucine at amino acid 260 of the envelope glycoprotein (GP). We also analyzed two additional CTL- variants and four spontaneous CTL+ revertants. All three CTL- variants differ from the original CTL+ parental strain at GP amino acid 260, indicating that this amino acid change is consistently associated with the CTL- phenotype. By contrast the other four mutations in LCMV are not associated with the CTL- phenotype. Sequence analysis of the coding regions of four CTL+ revertants of ARM clone 13 did not reveal back mutations at the GP 260 locus. This finding indicates that the GP 260 mutation is necessary but not sufficient for a CTL- P+ phenotype and that the reversion to CTL+ P- is likely either due to secondary mutations in other regions of the viral genome or to quasispecies within the revertant population that make significant contributions to the phenotype. | lld:pubmed |
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pubmed-article:1840619 | pubmed:language | eng | lld:pubmed |
pubmed-article:1840619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1840619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1840619 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1840619 | pubmed:month | Apr | lld:pubmed |
pubmed-article:1840619 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:1840619 | pubmed:author | pubmed-author:OldstoneM BMB | lld:pubmed |
pubmed-article:1840619 | pubmed:author | pubmed-author:SalvatoMM | lld:pubmed |
pubmed-article:1840619 | pubmed:author | pubmed-author:BorrowPP | lld:pubmed |
pubmed-article:1840619 | pubmed:author | pubmed-author:ShimomayeEE | lld:pubmed |
pubmed-article:1840619 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1840619 | pubmed:volume | 65 | lld:pubmed |
pubmed-article:1840619 | pubmed:owner | NLM | lld:pubmed |