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- W4313356504 abstract "Abstract Viral infections in the central nervous system (CNS) are associated with devastating neurological consequences in newborns. This may be due, in part, to deficiencies in the immature innate and adaptive immune response. To study viral CNS infections in neonates, we use a transgenic mouse model of neuronally-restricted measles virus (MV) infection (NSE-CD46 mice), where the human isoform of CD46, a MV receptor, is expressed under the control of the neuron-specific enolase promoter. Adult CD46+ mice survive infection and clear MV in an interferon gamma (IFNg)- and T cell-dependent manner. In contrast, neonatal CD46+ mice succumb to the infection despite T cell infiltration into the brain parenchyma. Neonatal mice lacking IFNg succumb more rapidly than wildtype pups despite higher T cell infiltration, equivalent natural killer cell infiltration, and microglial activation. Quantitative RT-PCR analysis demonstrated upregulation of pro-inflammatory cytokines and chemokines such as IFNg, IL-1β, and CXCL10, as well as the anti-inflammatory interleukin 1 receptor antagonist in infected adults and neonates. IL-12β, IL-23, CCL2, and TNF were significantly upregulated in infected neonates only. These results suggest the neonates are capable of cytokine production with a Th1-like profile within the CNS, but that the cytokine milieu is ineffective at controlling MV spread. Current experiments aim to inhibit inflammatory mediators such as CXCL10 and CCL2 that are expressed in an age-dependent manner during infection to determine if there is an improvement in neuropathology and survival of neonates." @default.
- W4313356504 created "2023-01-06" @default.
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- W4313356504 date "2016-05-01" @default.
- W4313356504 modified "2023-09-27" @default.
- W4313356504 title "Failure to control measles virus spread in the neonatal CNS despite immune cell infiltration and cytokine production." @default.
- W4313356504 doi "https://doi.org/10.4049/jimmunol.196.supp.217.24" @default.
- W4313356504 hasPublicationYear "2016" @default.
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