| pubmed-article:18094188 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C1175743 | lld:lifeskim |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C0014609 | lld:lifeskim |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C2936413 | lld:lifeskim |
| pubmed-article:18094188 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18094188 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:18094188 | pubmed:dateCreated | 2008-2-12 | lld:pubmed |
| pubmed-article:18094188 | pubmed:abstractText | In 2003, severe acute respiratory syndrome coronavirus (SARS-CoV) emerged and caused over 8,000 human cases of infection and more than 700 deaths worldwide. Zoonotic SARS-CoV likely evolved to infect humans by a series of transmission events between humans and animals for sale in China. Using synthetic biology, we engineered the spike protein (S) from a civet strain, SZ16, into our epidemic strain infectious clone, creating the chimeric virus icSZ16-S, which was infectious but yielded progeny viruses incapable of propagating in vitro. After introducing a K479N mutation within the S receptor binding domain (RBD) of SZ16, the recombinant virus (icSZ16-S K479N) replicated in Vero cells but was severely debilitated in growth. The in vitro evolution of icSZ16-S K479N on human airway epithelial (HAE) cells produced two viruses (icSZ16-S K479N D8 and D22) with enhanced growth on HAE cells and on delayed brain tumor cells expressing the SARS-CoV receptor, human angiotensin I converting enzyme 2 (hACE2). The icSZ16-S K479N D8 and D22 virus RBDs contained mutations in ACE2 contact residues, Y442F and L472F, that remodeled S interactions with hACE2. Further, these viruses were neutralized by a human monoclonal antibody (MAb), S230.15, but the parent icSZ16-S K479N strain was eight times more resistant than the mutants. These data suggest that the human adaptation of zoonotic SARS-CoV strains may select for some variants that are highly susceptible to select MAbs that bind to RBDs. The epidemic, icSZ16-S K479N, and icSZ16-S K479N D22 viruses replicate similarly in the BALB/c mouse lung, highlighting the potential use of these zoonotic spike SARS-CoVs to assess vaccine or serotherapy efficacy in vivo. | lld:pubmed |
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| pubmed-article:18094188 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18094188 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18094188 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18094188 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18094188 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18094188 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:18094188 | pubmed:issn | 1098-5514 | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:DonaldsonEric... | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:RockxBarryB | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:BaricRalphR | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:SimsAmyA | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:SheahanTimoth... | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:CortiDavideD | lld:pubmed |
| pubmed-article:18094188 | pubmed:author | pubmed-author:PicklesRaymon... | lld:pubmed |
| pubmed-article:18094188 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18094188 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:18094188 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18094188 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18094188 | pubmed:pagination | 2274-85 | lld:pubmed |
| pubmed-article:18094188 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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