| pubmed-article:15308716 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15308716 | lifeskim:mentions | umls-concept:C0682455 | lld:lifeskim |
| pubmed-article:15308716 | lifeskim:mentions | umls-concept:C0442886 | lld:lifeskim |
| pubmed-article:15308716 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:15308716 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:15308716 | pubmed:dateCreated | 2004-8-13 | lld:pubmed |
| pubmed-article:15308716 | pubmed:abstractText | Kaposi's sarcoma-associated herpesvirus and murine gammaherpesvirus-68 (MHV-68) establish latent infections and are associated with various types of malignancies. They are members of the gamma-2 herpesvirus subfamily and encode a replication and transcriptional activator, RTA, which is necessary and sufficient to disrupt latency and initiate the viral lytic cycle in vitro. We have constructed a recombinant MHV-68 virus that overexpresses RTA. This virus has faster replication kinetics in vitro and in vivo, is deficient in establishing latency, exhibits a reduction in the development of a mononucleosis-like disease in mice, and can protect mice against challenge by wild-type MHV-68. The present study, by using MHV-68 as an in vivo model system, demonstrated that RTA plays a critical role in the control of viral latency and suggests that latency is a determinant of viral pathogenesis in vivo. | lld:pubmed |
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| pubmed-article:15308716 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15308716 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15308716 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15308716 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15308716 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:BrownHelen... | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:SunRenR | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:WuTing-TingTT | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:Martinez-Guzm... | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:ColeStevenS | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:TongLemingL | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:RickabaughTam... | lld:pubmed |
| pubmed-article:15308716 | pubmed:author | pubmed-author:YuFuquF | lld:pubmed |
| pubmed-article:15308716 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15308716 | pubmed:volume | 78 | lld:pubmed |
| pubmed-article:15308716 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15308716 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15308716 | pubmed:pagination | 9215-23 | lld:pubmed |
| pubmed-article:15308716 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:15308716 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15308716 | pubmed:articleTitle | Generation of a latency-deficient gammaherpesvirus that is protective against secondary infection. | lld:pubmed |
| pubmed-article:15308716 | pubmed:affiliation | Molecular Biology Institute, University of California at Los Angeles, Los Angeles, California, USA. | lld:pubmed |
| pubmed-article:15308716 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15308716 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15308716 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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