pubmed-article:18801550 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C1175743 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C0152035 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C0024398 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C0024400 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C0960880 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C0183683 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
pubmed-article:18801550 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
pubmed-article:18801550 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18801550 | pubmed:dateCreated | 2008-10-28 | lld:pubmed |
pubmed-article:18801550 | pubmed:abstractText | Angiotensin converting enzyme 2 (ACE2) is the receptor that severe acute respiratory syndrome coronavirus (SARS-CoV) utilizes for target cell entry and, therefore, plays an important role in SARS pathogenesis. Since Chinese rhesus (rh) macaques do not usually develop SARS after SARS-CoV infection, it has been suggested that rh-ACE2 probably does not support viral entry efficiently. To determine the role of rh-ACE2 in early lung pathogenesis in vivo, we studied eleven Chinese rhesus monkeys experimentally infected with a pathogenic SARS-CoV(PUMC01) strain. Rh-ACE2 genes were amplified from all animals by reverse transcription polymerase chain reaction, and their function was studied in vitro using a pseudovirus entry assay. Many natural non-synonymous (NS) changes were found in rh-ACE2 genes. Compared to human (hu) ACE2, thirty-eight consensus NS changes were found in rh-ACE2. Since these changes do not interact with the receptor binding domain of SARS-CoV, rh-ACE2 in general is as effective as human homolog in supporting viral entry. Rh-ACE2, however, is more polymorphic than hu-ACE2. Additional sporadic NS substitutions in clone Rh11-7 reduced the level of rh-ACE2 protein expression and did not support viral entry effectively. Further mutagenesis analysis showed that a natural mutation Y217N dramatically alters ACE2 expression and entry efficiency. Moreover, introduction of the Y217N mutation into hu-ACE2 caused the down-regulation of expression and reduced viral entry efficiency. These results indicate that the Y217N mutation plays a role in modulating SARS-CoV infection. Our results provide insights for understanding the role of rh-ACE2 in SARS lung pathogenesis in a non-human primate model. | lld:pubmed |
pubmed-article:18801550 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18801550 | pubmed:language | eng | lld:pubmed |
pubmed-article:18801550 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18801550 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18801550 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18801550 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18801550 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18801550 | pubmed:month | Nov | lld:pubmed |
pubmed-article:18801550 | pubmed:issn | 1096-0341 | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:JosKK | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:HongJiangJ | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:ZhuHuaH | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:ChenZhiweiZ | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:QiangWeiW | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:QinChuanC | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:TuXinmingX | lld:pubmed |
pubmed-article:18801550 | pubmed:author | pubmed-author:ChenYunxinY | lld:pubmed |
pubmed-article:18801550 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18801550 | pubmed:day | 10 | lld:pubmed |
pubmed-article:18801550 | pubmed:volume | 381 | lld:pubmed |
pubmed-article:18801550 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18801550 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18801550 | pubmed:pagination | 89-97 | lld:pubmed |
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pubmed-article:18801550 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18801550 | pubmed:articleTitle | Rhesus angiotensin converting enzyme 2 supports entry of severe acute respiratory syndrome coronavirus in Chinese macaques. | lld:pubmed |
pubmed-article:18801550 | pubmed:affiliation | Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Peking Union Medical College, No.5, Panjiayuan, Nanli, Chaoyang District, Beijing, China. | lld:pubmed |
pubmed-article:18801550 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18801550 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:18801550 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:712790 | entrezgene:pubmed | pubmed-article:18801550 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:18801550 | lld:entrezgene |