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Cytokine Growth Factor Rev. 2014 Oct;25(5):525-31. doi: 10.1016/j.cytogfr.2014.07.002. Epub 2014 Jul 11.

Danger, diversity and priming in innate antiviral immunity.

Author information

1
Department of Pathology and Molecular Medicine, McMaster Immunology Research Center, Institute for Infectious Disease Research, McMaster University, Hamilton, Canada L8S 4K1.
2
Department of Pathology and Molecular Medicine, McMaster Immunology Research Center, Institute for Infectious Disease Research, McMaster University, Hamilton, Canada L8S 4K1. Electronic address: mossk@mcmaster.ca.

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.

KEYWORDS:

Danger; Interferon regulatory factors; Interferon-independent; Intrinsic and innate immunity; Priming

PMID:
25081316
DOI:
10.1016/j.cytogfr.2014.07.002
[Indexed for MEDLINE]

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