| pubmed-article:10864685 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10864685 | lifeskim:mentions | umls-concept:C0206679 | lld:lifeskim |
| pubmed-article:10864685 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
| pubmed-article:10864685 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10864685 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:10864685 | lifeskim:mentions | umls-concept:C0872054 | lld:lifeskim |
| pubmed-article:10864685 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:10864685 | pubmed:dateCreated | 2000-8-22 | lld:pubmed |
| pubmed-article:10864685 | pubmed:abstractText | Murine models of gamma interferon (IFN-gamma) deficiency demonstrate the role of this cytokine in attenuating acute herpes simplex virus (HSV) disease; however, the effect of IFN-gamma on the establishment and maintenance of neuronal latency and viral reactivation is not known. Using the IFN-gamma knockout (GKO) model of IFN-gamma deficiency and sensitive quantitative PCR methods, we show that IFN-gamma significantly reduces the ganglion content of latent HSV-1 in BALB/c mice, which in turn delays viral time to reactivation following UV irradiation. Similar effects were not seen in the C57BL/6 strain. These results indicate that IFN-gamma significantly attenuates latent HSV infection in the mouse model of ocular infection but has no impact on the maintenance of latency or virus reactivation. | lld:pubmed |
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| pubmed-article:10864685 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10864685 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10864685 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10864685 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10864685 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:10864685 | pubmed:author | pubmed-author:StrausS ESE | lld:pubmed |
| pubmed-article:10864685 | pubmed:author | pubmed-author:LeBlancR ARA | lld:pubmed |
| pubmed-article:10864685 | pubmed:author | pubmed-author:Lekstrom-Hime... | lld:pubmed |
| pubmed-article:10864685 | pubmed:author | pubmed-author:PesnicakLL | lld:pubmed |
| pubmed-article:10864685 | pubmed:author | pubmed-author:GodleskiMM | lld:pubmed |
| pubmed-article:10864685 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10864685 | pubmed:volume | 74 | lld:pubmed |
| pubmed-article:10864685 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10864685 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10864685 | pubmed:pagination | 6680-3 | lld:pubmed |
| pubmed-article:10864685 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10864685 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10864685 | pubmed:articleTitle | Gamma interferon impedes the establishment of herpes simplex virus type 1 latent infection but has no impact on its maintenance or reactivation in mice. | lld:pubmed |
| pubmed-article:10864685 | pubmed:affiliation | Medical Virology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. | lld:pubmed |
| pubmed-article:10864685 | pubmed:publicationType | Journal Article | lld:pubmed |
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