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1 Protects Mice from Acute Ocular Herpes Simplex Virus Type 1 Infection1
Department of Microbiology, Immunology, and Parasitology, Louisiana State University Medical Center, New Orleans, LA 70112; and Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037
Type I IFNs (i.e., IFN-
and IFN-ß) play a key role in the
host’s innate defense against viral pathogens. To examine the biologic
relevance of IFN- to a viral pathogen within the confines of the
nervous system, IFN-1 transgenic mice whose transgene is under the
control of the glial fibrillary acidic protein promoter (GFAP-IFN-,
astrocyte specific) were examined for resistance to an ocular herpes
simplex virus type 1 (HSV-1) infection. GFAP-IFN- mice expressed
significantly higher levels of IFN-ß (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-
,
and IFN- mRNA levels were reduced in the trigeminal ganglion of
GFAP-IFN- 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- 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- mice screened showed seroconversion by day
30 postinfection compared with nine of ten wild-type mice screened.
Collectively, the results show that the IFN-1 transgenic mice are
less susceptible to acute HSV-1 infection and the establishment of
viral latency.
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