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Autophagy receptors as viral targets

Activation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immu...

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Autor principal: Ylä-Anttila, Päivi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222950/
https://www.ncbi.nlm.nih.gov/pubmed/34167456
http://dx.doi.org/10.1186/s11658-021-00272-x
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author Ylä-Anttila, Päivi
author_facet Ylä-Anttila, Päivi
author_sort Ylä-Anttila, Päivi
collection PubMed
description Activation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immune responses, this autophagic elimination of foreign components is selective and requires specialized cargo receptors that function as links between a tagged foreign component and the autophagic machinery. Pathogens have evolved ways to evade their autophagic degradation to promote their replication, and recent research has shown autophagic receptors to be an important and perhaps previously overlooked target of viral autophagy inhibition. This is a brief summary of the recent progress in knowledge of virus-host interaction in the context of autophagy receptors.
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spelling pubmed-82229502021-06-24 Autophagy receptors as viral targets Ylä-Anttila, Päivi Cell Mol Biol Lett Review Letter Activation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immune responses, this autophagic elimination of foreign components is selective and requires specialized cargo receptors that function as links between a tagged foreign component and the autophagic machinery. Pathogens have evolved ways to evade their autophagic degradation to promote their replication, and recent research has shown autophagic receptors to be an important and perhaps previously overlooked target of viral autophagy inhibition. This is a brief summary of the recent progress in knowledge of virus-host interaction in the context of autophagy receptors. BioMed Central 2021-06-24 /pmc/articles/PMC8222950/ /pubmed/34167456 http://dx.doi.org/10.1186/s11658-021-00272-x Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Letter
Ylä-Anttila, Päivi
Autophagy receptors as viral targets
title Autophagy receptors as viral targets
title_full Autophagy receptors as viral targets
title_fullStr Autophagy receptors as viral targets
title_full_unstemmed Autophagy receptors as viral targets
title_short Autophagy receptors as viral targets
title_sort autophagy receptors as viral targets
topic Review Letter
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222950/
https://www.ncbi.nlm.nih.gov/pubmed/34167456
http://dx.doi.org/10.1186/s11658-021-00272-x
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