Defective NF-κB activation in virus-infected neuronal cells is restored by genetic complementation
Tóm tắt
The interferon-beta (IFNβ) gene is not inducible in neuronal cells in response to measles virus (MV) due to lack of nuclear factor kappa B (NF-κB) activation. NF-κB is normally sequestered in the cytoplasm by an inhibitor (IκBα). Previously, the authors demonstrated that the failure to activate neuronal NF-κB by MV was due to the inability to phosphorylate and degrade its inhibitor, IκBα. Here the authors demonstrate that transient transfection of a brain cDNA library into neuronal cells restores the ability of MV to activate NF-κB. In addition, tumor necrosis factor-alpha (TNFαb), but not interleukin-1 (IL-1) or lipopolysaccharide (LPS), stimulation resulted in IκBα phosphorylation and degradation in two neuronal cell lines. These results indicate that failure of MV to activate neuronal NF-κB is due to a signaling defect and that MV utilizes an NF-κB signaling pathway distinct from that of TNFα, but may overlap with that for IL-l and LPS.
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