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- W2025861570 abstract "The prototypic response to viral infection involves the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), leading to the activation of transcription factors such as IRF3 and NFkB and production of type 1 IFN. While this response can lead to the induction of hundreds of IFN-stimulated genes (ISGs) and recruitment and activation of immune cells, such a comprehensive response is likely inappropriate for routine low level virus exposure. Moreover, viruses have evolved a plethora of immune evasion strategies to subvert antiviral signalling. There is emerging evidence that cells have developed very sensitive methods of detecting not only specific viral PAMPS, but also more general danger or stress signals associated with viral entry and replication. Such stress-induced cellular responses likely serve to prime cells to respond to further PAMP stimulation or allow for a rapid and localized intracellular response independent of IFN production and its potential immune sequelae. This review discusses diversity in innate antiviral players and pathways, the role of danger sensing, and how alternative pathways, such as the IFN-independent pathway, may serve to prime cells for further pathogen attack." @default.
- W2025861570 created "2016-06-24" @default.
- W2025861570 creator A5019760105 @default.
- W2025861570 creator A5078849862 @default.
- W2025861570 date "2014-10-01" @default.
- W2025861570 modified "2023-10-02" @default.
- W2025861570 title "Danger, diversity and priming in innate antiviral immunity" @default.
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- W2025861570 doi "https://doi.org/10.1016/j.cytogfr.2014.07.002" @default.
- W2025861570 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25081316" @default.
- W2025861570 hasPublicationYear "2014" @default.
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