Endosomal Cholesterol in Viral Infections – A Common Denominator?

Cholesterol has gained tremendous attention as an essential lipid in the life cycle of virtually all viruses. These seem to have developed manifold strategies to modulate the cholesterol metabolism to the side of lipid uptake and de novo synthesis. In turn, affecting the cholesterol homeostasis has...

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Autores principales:	Mirco Glitscher, Eberhard Hildt
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	cholesterol trafficking viruses endosomes antivirals host-factors Physiology QP1-981
Acceso en línea:	https://doaj.org/article/95639d6952f842458c3da267067c6107
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spelling	oai:doaj.org-article:95639d6952f842458c3da267067c61072021-11-11T06:50:45ZEndosomal Cholesterol in Viral Infections – A Common Denominator?1664-042X10.3389/fphys.2021.750544https://doaj.org/article/95639d6952f842458c3da267067c61072021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.750544/fullhttps://doaj.org/toc/1664-042XCholesterol has gained tremendous attention as an essential lipid in the life cycle of virtually all viruses. These seem to have developed manifold strategies to modulate the cholesterol metabolism to the side of lipid uptake and de novo synthesis. In turn, affecting the cholesterol homeostasis has emerged as novel broad-spectrum antiviral strategy. On the other hand, the innate immune system is similarly regulated by the lipid and stimulated by its derivatives. This certainly requires attention in the design of antiviral strategies aiming to decrease cellular cholesterol, as evidence accumulates that withdrawal of cholesterol hampers innate immunity. Secondly, there are exceptions to the rule of the abovementioned virus-induced metabolic shift toward cholesterol anabolism. It therefore is of interest to dissect underlying regulatory mechanisms, which we aimed for in this minireview. We further collected evidence for intracellular cholesterol concentrations being less important in viral life cycles as compared to the spatial distribution of the lipid. Various routes of cholesterol trafficking were found to be hijacked in viral infections with respect to organelle-endosome contact sites mediating cholesterol shuttling. Thus, re-distribution of cellular cholesterol in the context of viral infections requires more attention in ongoing research. As a final aim, a pan-antiviral treatment could be found just within the transport and re-adjustment of local cholesterol concentrations. Thus, we aimed to emphasize the importance of the regulatory roles the endosomal system fulfils herein and hope to stimulate research in this field.Mirco GlitscherEberhard HildtFrontiers Media S.A.articlecholesteroltraffickingvirusesendosomesantiviralshost-factorsPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	cholesterol trafficking viruses endosomes antivirals host-factors Physiology QP1-981
spellingShingle	cholesterol trafficking viruses endosomes antivirals host-factors Physiology QP1-981 Mirco Glitscher Eberhard Hildt Endosomal Cholesterol in Viral Infections – A Common Denominator?
description	Cholesterol has gained tremendous attention as an essential lipid in the life cycle of virtually all viruses. These seem to have developed manifold strategies to modulate the cholesterol metabolism to the side of lipid uptake and de novo synthesis. In turn, affecting the cholesterol homeostasis has emerged as novel broad-spectrum antiviral strategy. On the other hand, the innate immune system is similarly regulated by the lipid and stimulated by its derivatives. This certainly requires attention in the design of antiviral strategies aiming to decrease cellular cholesterol, as evidence accumulates that withdrawal of cholesterol hampers innate immunity. Secondly, there are exceptions to the rule of the abovementioned virus-induced metabolic shift toward cholesterol anabolism. It therefore is of interest to dissect underlying regulatory mechanisms, which we aimed for in this minireview. We further collected evidence for intracellular cholesterol concentrations being less important in viral life cycles as compared to the spatial distribution of the lipid. Various routes of cholesterol trafficking were found to be hijacked in viral infections with respect to organelle-endosome contact sites mediating cholesterol shuttling. Thus, re-distribution of cellular cholesterol in the context of viral infections requires more attention in ongoing research. As a final aim, a pan-antiviral treatment could be found just within the transport and re-adjustment of local cholesterol concentrations. Thus, we aimed to emphasize the importance of the regulatory roles the endosomal system fulfils herein and hope to stimulate research in this field.
format	article
author	Mirco Glitscher Eberhard Hildt
author_facet	Mirco Glitscher Eberhard Hildt
author_sort	Mirco Glitscher
title	Endosomal Cholesterol in Viral Infections – A Common Denominator?
title_short	Endosomal Cholesterol in Viral Infections – A Common Denominator?
title_full	Endosomal Cholesterol in Viral Infections – A Common Denominator?
title_fullStr	Endosomal Cholesterol in Viral Infections – A Common Denominator?
title_full_unstemmed	Endosomal Cholesterol in Viral Infections – A Common Denominator?
title_sort	endosomal cholesterol in viral infections – a common denominator?
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/95639d6952f842458c3da267067c6107
work_keys_str_mv	AT mircoglitscher endosomalcholesterolinviralinfectionsacommondenominator AT eberhardhildt endosomalcholesterolinviralinfectionsacommondenominator
_version_	1718439422155816960

Endosomal Cholesterol in Viral Infections – A Common Denominator?

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