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• W4313333711 endingPage "4865" @default.
• W4313333711 startingPage "4859" @default.
• W4313333711 abstract "Abstract Type I IFNs (i.e., IFN-α and IFN-β) play a key role in the host’s innate defense against viral pathogens. To examine the biologic relevance of IFN-α to a viral pathogen within the confines of the nervous system, IFN-α1 transgenic mice whose transgene is under the control of the glial fibrillary acidic protein promoter (GFAP-IFN-α, astrocyte specific) were examined for resistance to an ocular herpes simplex virus type 1 (HSV-1) infection. GFAP-IFN-α mice expressed significantly higher levels of IFN-αβ (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-γ, and IFN-α mRNA levels were reduced in the trigeminal ganglion of GFAP-IFN-α 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-α 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-α mice screened showed seroconversion by day 30 postinfection compared with nine of ten wild-type mice screened. Collectively, the results show that the IFN-α1 transgenic mice are less susceptible to acute HSV-1 infection and the establishment of viral latency." @default.
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• W4313333711 date "1998-11-01" @default.
• W4313333711 modified "2023-10-11" @default.
• W4313333711 title "Astrocyte-Targeted Expression of IFN-α1 Protects Mice from Acute Ocular Herpes Simplex Virus Type 1 Infection" @default.
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• W4313333711 doi "https://doi.org/10.4049/jimmunol.161.9.4859" @default.
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