Influenza viruses and the NF-κB signaling pathway – towards a novel concept of antiviral therapy
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Abstract
Influenza A virus remains a major public health concern, both in its annual toll in death and debilitation and its potential to cause devastating pandemics. Like any other virus, influenza A viruses are strongly dependent on cellular factors for replication. One of the hallmark signaling factors activated by viral pathogens is the transcription factor NF-κB. Activation of NF-κB leads to the up-regulation of a variety of antiviral genes. Thus, the factor is commonly regarded as a major regulator of the innate immune defense to infection. However, several recent studies indicate that influenza viruses have acquired the capability to reprogram this antiviral activity and to exploit the factor for efficient replication. These data provide novel insights into the pathophysiological function of NF-κB in the special environment of a virus-infected cell. Furthermore, the unexpected viral dependency on a cellular signaling factor may pave the path for novel antiviral approaches targeting essential cellular components rather than viral factors.
©2008 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Guest Editorial
- Highlight – Viruses and Signaling
- Highlight: Viruses and Signaling
- HIV-1 at the immunological and T-lymphocytic virological synapse
- Pursuing different ‘TRADDes’: TRADD signaling induced by TNF-receptor 1 and the Epstein-Barr virus oncoprotein LMP1
- RNA viruses and the mitogenic Raf/MEK/ERK signal transduction cascade
- Hepatitis C virus (HCV) employs multiple strategies to subvert the host innate antiviral response
- Sabotage of antiviral signaling and effectors by influenza viruses
- Influenza viruses and the NF-κB signaling pathway – towards a novel concept of antiviral therapy
- Genes and Nucleic Acids
- Specific inhibition of transcriptional activity of the constitutive androstane receptor (CAR) by the splicing factor SF3a3
- Generation of synthetic RNA-based thermosensors
- Molecular Medicine
- Impaired synthesis of heme oxygenase-1 in Fanconi anemia cells can be rescued by transfection of Fanconi wild-type cDNA
- Cell Biology and Signaling
- Effects of the Cdc2-like kinase-family and DNA topoisomerase I on the alternative splicing of eNOS in TNF-α-stimulated human endothelial cells
- Proteolysis
- Cytotoxic and peptidase inhibitory activities of selected non-hepatotoxic cyclic peptides from cyanobacteria
