2009
DOI: 10.4049/jimmunol.0800596
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Local Type I IFN Receptor Signaling Protects against Virus Spread within the Central Nervous System

Abstract: Several neurotropic viruses such as vesicular stomatitis virus (VSV) induce peripheral neutralizing Ab responses and still can infect cells within the CNS. To address whether local type I IFN receptor (IFNAR) triggering plays a role in controlling virus replication within the brain, we generated mice with a cell type-specific IFNAR deletion in neuroectodermal cells of the CNS (NesCre+/−IFNARflox/flox). Intranasal VSV infection with 103 PFU was well tolerated by wild-type mice, whereas conventional IFNAR−/− mic… Show more

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Cited by 137 publications
(158 citation statements)
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“…Nevertheless, it is also possible that the protective role of increased IFN-␣ levels in the knockout mice is at the interface of the periphery and the central nervous system, af-fecting the as-yet poorly understood process of Sindbis virus neuroinvasion. For example, it has been reported that upon intranasal VSV instillation, early IFN response in the glomerular layer of the olfactory bulb is critically required to prevent viral spread over the entire CNS and thus confers survival (41). The mechanism by which increased early IFN-␣ levels lead to better control of Sindbis virus neuroinvasive disease is an interesting area for future investigation.…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, it is also possible that the protective role of increased IFN-␣ levels in the knockout mice is at the interface of the periphery and the central nervous system, af-fecting the as-yet poorly understood process of Sindbis virus neuroinvasion. For example, it has been reported that upon intranasal VSV instillation, early IFN response in the glomerular layer of the olfactory bulb is critically required to prevent viral spread over the entire CNS and thus confers survival (41). The mechanism by which increased early IFN-␣ levels lead to better control of Sindbis virus neuroinvasive disease is an interesting area for future investigation.…”
Section: Discussionmentioning
confidence: 99%
“…instillation, VSV infects olfactory sensory neurons in the nasal mucosa and moves along axons to the glomerular layer of the olfactory bulb. There, virus spread is efficiently arrested by a type I interferon (IFN)-dependent mechanism (4). Activation of astrocytes and astrogliosis were observed as early as 1 day postinfection (p.i.)…”
mentioning
confidence: 99%
“…To evaluate the influence of the infection route on IFN-␤ production in the central nervous system (CNS), we performed intranasal infections with a recombinant RABV carrying the G protein of the more neurotropic CVS strain (SAD-G CVS ) and vesicular stomatitis virus (VSV) strain Indiana, both of which can infect mice via the intranasal route (4,18). Rabies virus induced the luciferase reporter gene in all brain parts of ⌬␤-luc reporter mice, whereas reporter gene expression in VSV-infected mice was restricted to the olfactory bulb (data not shown).…”
Section: Astrocytes Are the Main Ifn-␤ Producers During Intracranial mentioning
confidence: 99%
“…IFN-based mechanisms can restrict viral replication in the brain (3). Using mice lacking functional IFN receptors specifically on neuroectodermal cells, it could be shown that a local IFN response in the brain is required to block the spread of vesicular stomatitis virus (VSV) (4). Interestingly, however, dedicated IFN producer cells such as plasmacytoid dendritic cells are absent from the brain parenchyma (5).…”
mentioning
confidence: 99%