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Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis
It is well-known that viruses activate various inflammasomes, which can initiate the programmed cell death pathway known as pyroptosis, subsequently leading to cell lysis and release of inflammatory cytokines IL-1 [Formula: see text] and IL-18. This pathway can be triggered by various sensors, inclu...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9609106/ https://www.ncbi.nlm.nih.gov/pubmed/36298668 http://dx.doi.org/10.3390/v14102113 |
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author | Wallace, Hannah L. Russell, Rodney S. |
author_facet | Wallace, Hannah L. Russell, Rodney S. |
author_sort | Wallace, Hannah L. |
collection | PubMed |
description | It is well-known that viruses activate various inflammasomes, which can initiate the programmed cell death pathway known as pyroptosis, subsequently leading to cell lysis and release of inflammatory cytokines IL-1 [Formula: see text] and IL-18. This pathway can be triggered by various sensors, including, but not limited to, NLRP3, AIM2, IFI16, RIG-I, and NLRC4. Many viruses are known either to activate or inhibit inflammasomes as a part of the innate immune response or as a mechanism of pathogenesis. Early research in the field of virus-induced pyroptosis suggested a dichotomy, with RNA viruses activating the NLRP3 inflammasome and DNA viruses activating the AIM2 inflammasome. More recent research has shown that this dichotomy may not be as distinct as once thought. It seems many viruses activate multiple inflammasome sensors. Here, we detail which viruses fit the dichotomy as well as many that appear to defy this clearly false dichotomy. It seems likely that most, if not all, viruses activate multiple inflammasome sensors, and future research should focus on expanding our understanding of inflammasome activation in a variety of tissue types as well as virus activation of multiple inflammasomes, challenging biases that stemmed from early literature in this field. Here, we review primarily research performed on human viruses but also include details regarding animal viruses whenever possible. |
format | Online Article Text |
id | pubmed-9609106 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-96091062022-10-28 Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis Wallace, Hannah L. Russell, Rodney S. Viruses Review It is well-known that viruses activate various inflammasomes, which can initiate the programmed cell death pathway known as pyroptosis, subsequently leading to cell lysis and release of inflammatory cytokines IL-1 [Formula: see text] and IL-18. This pathway can be triggered by various sensors, including, but not limited to, NLRP3, AIM2, IFI16, RIG-I, and NLRC4. Many viruses are known either to activate or inhibit inflammasomes as a part of the innate immune response or as a mechanism of pathogenesis. Early research in the field of virus-induced pyroptosis suggested a dichotomy, with RNA viruses activating the NLRP3 inflammasome and DNA viruses activating the AIM2 inflammasome. More recent research has shown that this dichotomy may not be as distinct as once thought. It seems many viruses activate multiple inflammasome sensors. Here, we detail which viruses fit the dichotomy as well as many that appear to defy this clearly false dichotomy. It seems likely that most, if not all, viruses activate multiple inflammasome sensors, and future research should focus on expanding our understanding of inflammasome activation in a variety of tissue types as well as virus activation of multiple inflammasomes, challenging biases that stemmed from early literature in this field. Here, we review primarily research performed on human viruses but also include details regarding animal viruses whenever possible. MDPI 2022-09-23 /pmc/articles/PMC9609106/ /pubmed/36298668 http://dx.doi.org/10.3390/v14102113 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Wallace, Hannah L. Russell, Rodney S. Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title | Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title_full | Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title_fullStr | Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title_full_unstemmed | Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title_short | Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis |
title_sort | promiscuous inflammasomes: the false dichotomy of rna/dna virus-induced inflammasome activation and pyroptosis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9609106/ https://www.ncbi.nlm.nih.gov/pubmed/36298668 http://dx.doi.org/10.3390/v14102113 |
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