| pubmed-article:2539529 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C0318467 | lld:lifeskim |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C0067032 | lld:lifeskim |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C2936413 | lld:lifeskim |
| pubmed-article:2539529 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:2539529 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:2539529 | pubmed:dateCreated | 1989-5-18 | lld:pubmed |
| pubmed-article:2539529 | pubmed:abstractText | Human rhinovirus 39 (HRV39) is blocked in nonpermissive L cells at both adsorption and intracellular replication steps. We have selected a host range variant of HRV39 capable of bypassing the intracellular replication block and found it to have altered nonstructural P2 proteins. These alterations are similar to those reported earlier for host range variants of HRV2 (F. H. Yin and N. B. Lomax, J. Virol. 48:410-418, 1983). This observation suggests that the intracellular replication block for both HRV2 and HRV39 in mouse L cells is at the same step. We propose that the P2 protein is an essential viral component that cannot function in mouse L cells unless altered. This alteration occurs spontaneously in stocks of HRV39 during growth in permissive HeLa cells. | lld:pubmed |
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| pubmed-article:2539529 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2539529 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2539529 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2539529 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2539529 | pubmed:month | May | lld:pubmed |
| pubmed-article:2539529 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:2539529 | pubmed:author | pubmed-author:YinF HFH | lld:pubmed |
| pubmed-article:2539529 | pubmed:author | pubmed-author:LomaxN BNB | lld:pubmed |
| pubmed-article:2539529 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2539529 | pubmed:volume | 63 | lld:pubmed |
| pubmed-article:2539529 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2539529 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2539529 | pubmed:pagination | 2396-9 | lld:pubmed |
| pubmed-article:2539529 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2539529 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2539529 | pubmed:articleTitle | Evidence for the role of the P2 protein of human rhinovirus in its host range change. | lld:pubmed |
| pubmed-article:2539529 | pubmed:affiliation | Central Research and Development Department, E.I. du Pont de Nemours and Company, Wilmington, Delaware 19880-0328. | lld:pubmed |
| pubmed-article:2539529 | pubmed:publicationType | Journal Article | lld:pubmed |
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