Viral evasion and subversion of pattern-recognition receptor signalling
By A. Bowie, Leonie Unterholzner. Nature reviews. Immunology, 2008
775 citations recorded by the source corpus.
The expression of pattern-recognition receptors (PRRs) by immune and tissue cells provides the host with the ability to detect and respond to infection by viruses and other microorganisms. Significant progress has been made from studying this area, including the identification of PRRs, such as Toll-like receptors and RIG-I-like receptors, and the description of the molecular basis of their signalling pathways, which lead to the production of interferons and other cytokines. In parallel, common mechanisms used by viruses to evade PRR-mediated responses or to actively subvert these pathways for their own benefit are emerging. Accumulating evidence on how viral infection and PRR signalling pathways intersect is providing further insights into the function of the pathways involved, their constituent proteins and ways in which they could be manipulated therapeutically.
Subfields: Epidemiology, Immunology, Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/cec3aa6bf5a24cf092cff2d19709d22427bdb635
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Citations in the corpus
- Type I interferon: friend or foe? (2010, background): “Not surprisingly, many viruses have evolved molecular mechanisms to either prevent type I IFN induction or block the signaling through its receptors (Bowie and Unterholzner, 2008).”
- MicroRNA-146a Feedback Inhibits RIG-I-Dependent Type I IFN Production in Macrophages by Targeting TRAF6, IRAK1, and IRAK21 (2009, background): “Alternatively, viruses can disrupt the RIG-I signaling pathway and thus inhibit RIG-I-mediated antiviral activities in host cells through many viral components or responsive host negative regulators (8, 14).”
- A structure-based model of RIG-I activation. (2012, background): “immune pathways, see Bowie and Unterholzner (2008).”
- Crosstalk between nucleocytoplasmic trafficking and the innate immune response to viral infection (2021, background): “Consequently, this stimulates the production of proteins that establish a robust immune response to repress the replication and assembly of pathogens (99, 100).”
- Necroptosis: the release of damage-associated molecular patterns and its physiological relevance. (2013, background): “For example, protein A52R expressed by VV inhibits the signaling mediated by TLR2, 4, and 9, West Nile virus (WNV) nonstructural protein 1 (NS1) inhibits TLR3 signaling, and other viral proteins sequester virus dsRNA (Aravalli et al., 2008; Bowie and Unterholzner, 2008) (Figure 2B).”
- Mitochondria in innate immune responses (2011, background): “However, many viruses possess the ability to evade detection and/or suppress host innate antiviral immune responses, and several reports have uncovered viral evasion strategies involving suppression of MAVS signallin”
- Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms (2021, background): “Like all pathogens, SARS-CoV-2 employs a number of mechanisms to disable and evade the host immune response (Lucas et al., 2001; Bowie and Unterholzner, 2008; Taefehshokr et al., 2020).”