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| pubmed-article:1328671 | lifeskim:mentions | umls-concept:C0024398 | lld:lifeskim |
| pubmed-article:1328671 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:1328671 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
| pubmed-article:1328671 | lifeskim:mentions | umls-concept:C0796344 | lld:lifeskim |
| pubmed-article:1328671 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:1328671 | pubmed:dateCreated | 1992-11-18 | lld:pubmed |
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| pubmed-article:1328671 | pubmed:abstractText | Simian virus 40 (SV40) was isolated from the brains of three rhesus monkeys and the kidneys of two other rhesus monkeys with simian immunodeficiency virus-induced immunodeficiency. A striking feature of these five cases was the tissue specificity of the SV40 replication. SV40 was also isolated from the kidney of a Taiwanese rock macaque with immunodeficiency probably caused by type D retrovirus infection. Multiple full-length clones were derived from all six fresh SV40 isolates, and two separate regions of their genomes were sequenced: the origin (ori)-enhancer region and the coding region for the carboxy terminus of T antigen (T-ag). None of the 23 clones analyzed had two 72-bp enhancer elements as are present in the commonly used laboratory strain 776 of SV40; 22 of these 23 clones were identical in their ori-enhancer sequences, and these had only a single 72-bp enhancer element. We found no evidence for differences in ori-enhancer sequences associated with tissue-specific SV40 replication. The T-ag coding sequence that was analyzed was identical in all clones from kidney. However, significant variation was observed in the carboxy-terminal region of T-ag in SV40 isolated from brain tissues. This sequence variation was located in a region previously reported to be responsible for SV40 host range in cultured cell lines. Thus, SV40 appears to be an opportunistic pathogen in the setting of simian immunodeficiency virus-induced immunodeficiency, similarly to JC virus in human immunodeficiency virus-infected humans, the enhancer sequence organization generally attributed to SV40 is not representative of natural SV40 isolates, and sequence variation near the carboxy terminus of T-ag may play a role in tissue-specific replication of SV40. | lld:pubmed |
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| pubmed-article:1328671 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1328671 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1328671 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1328671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1328671 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1328671 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:1328671 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:1328671 | pubmed:author | pubmed-author:DanielM DMD | lld:pubmed |
| pubmed-article:1328671 | pubmed:author | pubmed-author:DesrosiersR... | lld:pubmed |
| pubmed-article:1328671 | pubmed:author | pubmed-author:IlyinskiiP... | lld:pubmed |
| pubmed-article:1328671 | pubmed:author | pubmed-author:HorvathC JCJ | lld:pubmed |
| pubmed-article:1328671 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1328671 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:1328671 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1328671 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1328671 | pubmed:pagination | 6353-60 | lld:pubmed |
| pubmed-article:1328671 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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