pubmed-article:3035217 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C0206558 | lld:lifeskim |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C0040995 | lld:lifeskim |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C0040077 | lld:lifeskim |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
pubmed-article:3035217 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:3035217 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:3035217 | pubmed:dateCreated | 1987-7-15 | lld:pubmed |
pubmed-article:3035217 | pubmed:abstractText | Infection of trigeminal ganglion by herpes simplex virus (HSV) thymidine kinase-negative (TK-) mutants was investigated in mixed infection studies in mice. Mice were corneally inoculated with TK- HSV alone or with mixtures of TK- HSV-TK+ HSV. When inoculated alone, an arabinosylthymine-selected HSV type 1 TK- mutant and a HSV type 2 TK- deletion mutant infected mouse ocular tissues but rarely infected ganglion tissues. However, both TK- mutants readily infected ganglion tissues when they were inoculated in mixtures with TK+ HSV. By means of mixed infection studies, it was demonstrated that TK- HSV could readily establish acute and latent ganglion infections. It was thought that the frequent infection of trigeminal ganglion tissue by both TK- mutants after mixed TK(-)-TK+ HSV infection was the result of in vivo complementation. After mixed TK(-)-TK+ HSV infection and subsequent cultivation of ganglion explants in arabinosylthymine, results supported the conclusion that when TK- was present in ganglia it was in the same neurons that contained TK+ HSV. | lld:pubmed |
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pubmed-article:3035217 | pubmed:language | eng | lld:pubmed |
pubmed-article:3035217 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3035217 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3035217 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3035217 | pubmed:month | Jul | lld:pubmed |
pubmed-article:3035217 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:3035217 | pubmed:author | pubmed-author:TenserR BRB | lld:pubmed |
pubmed-article:3035217 | pubmed:author | pubmed-author:EdrisW AWA | lld:pubmed |
pubmed-article:3035217 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3035217 | pubmed:volume | 61 | lld:pubmed |
pubmed-article:3035217 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3035217 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3035217 | pubmed:pagination | 2171-4 | lld:pubmed |
pubmed-article:3035217 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:3035217 | pubmed:year | 1987 | lld:pubmed |
pubmed-article:3035217 | pubmed:articleTitle | Trigeminal ganglion infection by thymidine kinase-negative mutants of herpes simplex virus after in vivo complementation. | lld:pubmed |
pubmed-article:3035217 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3035217 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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