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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1998-11-18
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pubmed:abstractText |
Type I IFNs (i.e., IFN-alpha and IFN-beta) play a key role in the host's innate defense against viral pathogens. To examine the biologic relevance of IFN-alpha to a viral pathogen within the confines of the nervous system, IFN-alpha1 transgenic mice whose transgene is under the control of the glial fibrillary acidic protein promoter (GFAP-IFN-alpha, astrocyte specific) were examined for resistance to an ocular herpes simplex virus type 1 (HSV-1) infection. GFAP-IFN-alpha mice expressed significantly higher levels of IFN-alphabeta (533 U) in the trigeminal ganglion compared with nontransgenic mice (70 U) 72 h postinfection that corresponded with a significant reduction in the mRNA expression of the HSV-1 immediate early gene infected cell polypeptide 27 and late gene VP16, as well as the chemokines monocyte-chemoattractant protein-1 and cytokine response gene-2 in the eye and trigeminal ganglion. Six days postinfection, the viral load and the expression of infected cell polypeptide 27, CD8, RANTES, IFN-gamma, and IFN-alpha mRNA levels were reduced in the trigeminal ganglion of GFAP-IFN-alpha mice compared with the wild-type mice. Following the establishment of HSV-1 latency (i.e., 30 days postinfection), only one of nine (11%) GFAP-IFN-alpha mice was found to be latent compared with seven of eight (88%) of the wild-type mice, as determined by the expression of the latency-associated transcript RNAs. Likewise, only three of nine GFAP-IFN-alpha mice screened showed seroconversion by day 30 postinfection compared with nine of ten wild-type mice screened. Collectively, the results show that the IFN-alpha1 transgenic mice are less susceptible to acute HSV-1 infection and the establishment of viral latency.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
161
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4859-65
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9794419-Animals,
pubmed-meshheading:9794419-Astrocytes,
pubmed-meshheading:9794419-Disease Susceptibility,
pubmed-meshheading:9794419-Gene Expression Regulation,
pubmed-meshheading:9794419-Glial Fibrillary Acidic Protein,
pubmed-meshheading:9794419-Interferon-alpha,
pubmed-meshheading:9794419-Keratitis, Herpetic,
pubmed-meshheading:9794419-Mice,
pubmed-meshheading:9794419-Mice, Transgenic,
pubmed-meshheading:9794419-RNA, Messenger,
pubmed-meshheading:9794419-Recombinant Fusion Proteins,
pubmed-meshheading:9794419-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:9794419-Simplexvirus,
pubmed-meshheading:9794419-Trigeminal Ganglion,
pubmed-meshheading:9794419-Virus Latency
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pubmed:year |
1998
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pubmed:articleTitle |
Astrocyte-targeted expression of IFN-alpha1 protects mice from acute ocular herpes simplex virus type 1 infection.
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pubmed:affiliation |
Department of Microbiology, Immunology, and Parasitology, Louisiana State University Medical Center, New Orleans 70112-1393, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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