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Inflammasome activation by viral infection: mechanisms of activation and regulation

Viral diseases are the most common problems threatening human health, livestock, and poultry industries worldwide. Viral infection is a complex and competitive dynamic biological process between a virus and a host/target cell. During viral infection, inflammasomes play important roles in the host an...

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Autores principales: Shi, Wen, Jin, Mengyun, Chen, Hao, Wu, Zongxue, Yuan, Liuyang, Liang, Si, Wang, Xiaohan, Memon, Fareed Uddin, Eldemery, Fatma, Si, Hongbin, Ou, Changbo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10440708/
https://www.ncbi.nlm.nih.gov/pubmed/37608944
http://dx.doi.org/10.3389/fmicb.2023.1247377
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author Shi, Wen
Jin, Mengyun
Chen, Hao
Wu, Zongxue
Yuan, Liuyang
Liang, Si
Wang, Xiaohan
Memon, Fareed Uddin
Eldemery, Fatma
Si, Hongbin
Ou, Changbo
author_facet Shi, Wen
Jin, Mengyun
Chen, Hao
Wu, Zongxue
Yuan, Liuyang
Liang, Si
Wang, Xiaohan
Memon, Fareed Uddin
Eldemery, Fatma
Si, Hongbin
Ou, Changbo
author_sort Shi, Wen
collection PubMed
description Viral diseases are the most common problems threatening human health, livestock, and poultry industries worldwide. Viral infection is a complex and competitive dynamic biological process between a virus and a host/target cell. During viral infection, inflammasomes play important roles in the host and confer defense mechanisms against the virus. Inflammasomes are polymeric protein complexes and are considered important components of the innate immune system. These immune factors recognize the signals of cell damage or pathogenic microbial infection after activation by the canonical pathway or non-canonical pathway and transmit signals to the immune system to initiate the inflammatory responses. However, some viruses inhibit the activation of the inflammasomes in order to replicate and proliferate in the host. In recent years, the role of inflammasome activation and/or inhibition during viral infection has been increasingly recognized. Therefore, in this review, we describe the biological properties of the inflammasome associated with viral infection, discuss the potential mechanisms that activate and/or inhibit NLRP1, NLRP3, and AIM2 inflammasomes by different viruses, and summarize the reciprocal regulatory effects of viral infection on the NLRP3 inflammasome in order to explore the relationship between viral infection and inflammasomes. This review will pave the way for future studies on the activation mechanisms of inflammasomes and provide novel insights for the development of antiviral therapies.
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spelling pubmed-104407082023-08-22 Inflammasome activation by viral infection: mechanisms of activation and regulation Shi, Wen Jin, Mengyun Chen, Hao Wu, Zongxue Yuan, Liuyang Liang, Si Wang, Xiaohan Memon, Fareed Uddin Eldemery, Fatma Si, Hongbin Ou, Changbo Front Microbiol Microbiology Viral diseases are the most common problems threatening human health, livestock, and poultry industries worldwide. Viral infection is a complex and competitive dynamic biological process between a virus and a host/target cell. During viral infection, inflammasomes play important roles in the host and confer defense mechanisms against the virus. Inflammasomes are polymeric protein complexes and are considered important components of the innate immune system. These immune factors recognize the signals of cell damage or pathogenic microbial infection after activation by the canonical pathway or non-canonical pathway and transmit signals to the immune system to initiate the inflammatory responses. However, some viruses inhibit the activation of the inflammasomes in order to replicate and proliferate in the host. In recent years, the role of inflammasome activation and/or inhibition during viral infection has been increasingly recognized. Therefore, in this review, we describe the biological properties of the inflammasome associated with viral infection, discuss the potential mechanisms that activate and/or inhibit NLRP1, NLRP3, and AIM2 inflammasomes by different viruses, and summarize the reciprocal regulatory effects of viral infection on the NLRP3 inflammasome in order to explore the relationship between viral infection and inflammasomes. This review will pave the way for future studies on the activation mechanisms of inflammasomes and provide novel insights for the development of antiviral therapies. Frontiers Media S.A. 2023-08-07 /pmc/articles/PMC10440708/ /pubmed/37608944 http://dx.doi.org/10.3389/fmicb.2023.1247377 Text en Copyright © 2023 Shi, Jin, Chen, Wu, Yuan, Liang, Wang, Memon, Eldemery, Si and Ou. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Shi, Wen
Jin, Mengyun
Chen, Hao
Wu, Zongxue
Yuan, Liuyang
Liang, Si
Wang, Xiaohan
Memon, Fareed Uddin
Eldemery, Fatma
Si, Hongbin
Ou, Changbo
Inflammasome activation by viral infection: mechanisms of activation and regulation
title Inflammasome activation by viral infection: mechanisms of activation and regulation
title_full Inflammasome activation by viral infection: mechanisms of activation and regulation
title_fullStr Inflammasome activation by viral infection: mechanisms of activation and regulation
title_full_unstemmed Inflammasome activation by viral infection: mechanisms of activation and regulation
title_short Inflammasome activation by viral infection: mechanisms of activation and regulation
title_sort inflammasome activation by viral infection: mechanisms of activation and regulation
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10440708/
https://www.ncbi.nlm.nih.gov/pubmed/37608944
http://dx.doi.org/10.3389/fmicb.2023.1247377
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