Home > Research > Publications & Outputs > The interplay between viruses and innate immune...

Links

Text available via DOI:

View graph of relations

The interplay between viruses and innate immune signaling: recent insights and therapeutic opportunities

Research output: Contribution to journalJournal articlepeer-review

Published

Standard

The interplay between viruses and innate immune signaling : recent insights and therapeutic opportunities. / Unterholzner, Leonie; Bowie, Andrew G.

In: Biochemical Pharmacology, Vol. 75, No. 3, 01.02.2008, p. 589-602.

Research output: Contribution to journalJournal articlepeer-review

Harvard

APA

Vancouver

Author

Unterholzner, Leonie ; Bowie, Andrew G. / The interplay between viruses and innate immune signaling : recent insights and therapeutic opportunities. In: Biochemical Pharmacology. 2008 ; Vol. 75, No. 3. pp. 589-602.

Bibtex

@article{2b73fa59fe9e4852ab0b0d5d76b72394,
title = "The interplay between viruses and innate immune signaling: recent insights and therapeutic opportunities",
abstract = "The immediate response to viral infection relies on pattern-recognition receptors (PRRs), most prominently the Toll-like receptors (TLRs) and the RNA helicases RIG-I and MDA5, as well as double stranded RNA-dependent protein kinase (PKR) and the DNA receptor, DAI. These PRRs recognize pathogen-associated molecular patterns (PAMPs) such as viral proteins and nucleic acids. The engagement of these receptors then initiates intracellular signaling cascades which ultimately cause the activation of transcription factors and the expression of type I interferons and pro-inflammatory cytokines. This innate response establishes an anti-viral state in the infected cell and its neighbours and alerts immune cells to the danger. In order to establish a productive infection, viruses need to overcome this initial anti-viral response. Evasion of innate immune defences is achieved by means of viral proteins that inhibit the signaling cascades emanating from the PRRs. The same innate signal transduction pathways have been implicated in conditions of sterile inflammation, such as rheumatoid arthritis and multiple sclerosis, and in autoimmunity. Because viral proteins target crucial host proteins involved in these pathways, they can point the way to key drug targets. Further, the viral proteins themselves or derivatives of them may be of use therapeutically to curtail inflammation and autoimmunity.",
keywords = "Animals, DEAD-box RNA Helicases, Humans, Immunity, Innate, Interferon Regulatory Factor-3, Interferon Regulatory Factor-7, NF-kappa B, Signal Transduction, Toll-Like Receptors, Virus Diseases, eIF-2 Kinase",
author = "Leonie Unterholzner and Bowie, {Andrew G.}",
year = "2008",
month = feb,
day = "1",
doi = "10.1016/j.bcp.2007.07.043",
language = "English",
volume = "75",
pages = "589--602",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - The interplay between viruses and innate immune signaling

T2 - recent insights and therapeutic opportunities

AU - Unterholzner, Leonie

AU - Bowie, Andrew G.

PY - 2008/2/1

Y1 - 2008/2/1

N2 - The immediate response to viral infection relies on pattern-recognition receptors (PRRs), most prominently the Toll-like receptors (TLRs) and the RNA helicases RIG-I and MDA5, as well as double stranded RNA-dependent protein kinase (PKR) and the DNA receptor, DAI. These PRRs recognize pathogen-associated molecular patterns (PAMPs) such as viral proteins and nucleic acids. The engagement of these receptors then initiates intracellular signaling cascades which ultimately cause the activation of transcription factors and the expression of type I interferons and pro-inflammatory cytokines. This innate response establishes an anti-viral state in the infected cell and its neighbours and alerts immune cells to the danger. In order to establish a productive infection, viruses need to overcome this initial anti-viral response. Evasion of innate immune defences is achieved by means of viral proteins that inhibit the signaling cascades emanating from the PRRs. The same innate signal transduction pathways have been implicated in conditions of sterile inflammation, such as rheumatoid arthritis and multiple sclerosis, and in autoimmunity. Because viral proteins target crucial host proteins involved in these pathways, they can point the way to key drug targets. Further, the viral proteins themselves or derivatives of them may be of use therapeutically to curtail inflammation and autoimmunity.

AB - The immediate response to viral infection relies on pattern-recognition receptors (PRRs), most prominently the Toll-like receptors (TLRs) and the RNA helicases RIG-I and MDA5, as well as double stranded RNA-dependent protein kinase (PKR) and the DNA receptor, DAI. These PRRs recognize pathogen-associated molecular patterns (PAMPs) such as viral proteins and nucleic acids. The engagement of these receptors then initiates intracellular signaling cascades which ultimately cause the activation of transcription factors and the expression of type I interferons and pro-inflammatory cytokines. This innate response establishes an anti-viral state in the infected cell and its neighbours and alerts immune cells to the danger. In order to establish a productive infection, viruses need to overcome this initial anti-viral response. Evasion of innate immune defences is achieved by means of viral proteins that inhibit the signaling cascades emanating from the PRRs. The same innate signal transduction pathways have been implicated in conditions of sterile inflammation, such as rheumatoid arthritis and multiple sclerosis, and in autoimmunity. Because viral proteins target crucial host proteins involved in these pathways, they can point the way to key drug targets. Further, the viral proteins themselves or derivatives of them may be of use therapeutically to curtail inflammation and autoimmunity.

KW - Animals

KW - DEAD-box RNA Helicases

KW - Humans

KW - Immunity, Innate

KW - Interferon Regulatory Factor-3

KW - Interferon Regulatory Factor-7

KW - NF-kappa B

KW - Signal Transduction

KW - Toll-Like Receptors

KW - Virus Diseases

KW - eIF-2 Kinase

U2 - 10.1016/j.bcp.2007.07.043

DO - 10.1016/j.bcp.2007.07.043

M3 - Journal article

C2 - 17868652

VL - 75

SP - 589

EP - 602

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

IS - 3

ER -