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Article ; Online: Virus-induced metabolic reprogramming and innate sensing hereof by the infected host.

Thyrsted, Jacob / Holm, Christian Kanstrup

2020 Volume 68, Page(s) 44–50

Abstract: To make new infectious particles, all viruses must manipulate host cell metabolism to secure sufficient availability of biomolecules and energy-a phenomenon now known as metabolic reprogramming. Numerous observations of this has already been made for a ... ...

Abstract	To make new infectious particles, all viruses must manipulate host cell metabolism to secure sufficient availability of biomolecules and energy-a phenomenon now known as metabolic reprogramming. Numerous observations of this has already been made for a range of viruses with each type of virus seemingly applying its own unique tactics to accomplish this unifying goal. In this light, metabolic reprogramming of the infected cell is largely beneficial to the virus and not to the host. On the other hand, virus-induced metabolic reprogramming represents a transformed self with distorted cellular and extracellular levels of distinct metabolites and metabolic by-products. This review briefly outlines current knowledge of virus-induced metabolic reprogramming, discusses how this could be sensed by the infected host to initiate anti-viral programs, and presents examples of innate anti-viral mechanisms of the host that target the availability of biomolecules to block viral replication.
MeSH term(s)	Host-Pathogen Interactions ; Immunity, Innate ; Virus Replication ; Viruses
Language	English
Publishing date	2020-10-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1052045-4
ISSN	1879-0429 ; 0958-1669
ISSN (online)	1879-0429
ISSN	0958-1669
DOI	10.1016/j.copbio.2020.10.004
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Zs.A 3071: Show issues

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Article: NRF2 in Viral Infection.

Herengt, Angela / Thyrsted, Jacob / Holm, Christian K

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 9

Abstract: The transcription factor NRF2 is central to redox homeostasis in animal cells and is a well-known driver of chemoresistance in many types of cancer. Recently, new roles have been ascribed to NRF2 which include regulation of antiviral interferon responses ...

Abstract	The transcription factor NRF2 is central to redox homeostasis in animal cells and is a well-known driver of chemoresistance in many types of cancer. Recently, new roles have been ascribed to NRF2 which include regulation of antiviral interferon responses and inflammation. In addition, NRF2 is emerging as an important factor in antiviral immunity through interferon-independent mechanisms. In the review, we give an overview of the scientific progress on the involvement and importance of NRF2 in the context of viral infection.
Language	English
Publishing date	2021-09-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091491
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Article: NRF2 in Viral Infection

Herengt, Angela / Thyrsted, Jacob / Holm, Christian K.

Antioxidants. 2021 Sept. 18, v. 10, no. 9

2021

Abstract	The transcription factor NRF2 is central to redox homeostasis in animal cells and is a well-known driver of chemoresistance in many types of cancer. Recently, new roles have been ascribed to NRF2 which include regulation of antiviral interferon responses and inflammation. In addition, NRF2 is emerging as an important factor in antiviral immunity through interferon-independent mechanisms. In the review, we give an overview of the scientific progress on the involvement and importance of NRF2 in the context of viral infection.
Keywords	homeostasis ; immunity ; inflammation ; interferons ; transcription factors
Language	English
Dates of publication	2021-0918
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091491
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Amyloid-β aggregates activate peripheral monocytes in mild cognitive impairment.

Nature communications

2024 Volume 15, Issue 1, Page(s) 1224

Abstract: The peripheral immune system is important in neurodegenerative diseases, both in protecting and inflaming the brain, but the underlying mechanisms remain elusive. Alzheimer's Disease is commonly preceded by a prodromal period. Here, we report the ... ...

Abstract	The peripheral immune system is important in neurodegenerative diseases, both in protecting and inflaming the brain, but the underlying mechanisms remain elusive. Alzheimer's Disease is commonly preceded by a prodromal period. Here, we report the presence of large Aβ aggregates in plasma from patients with mild cognitive impairment (n = 38). The aggregates are associated with low level Alzheimer's Disease-like brain pathology as observed by
MeSH term(s)	Humans ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Cognitive Dysfunction ; Integrin alphaXbeta2 ; Monocytes/pathology
Chemical Substances	Amyloid beta-Peptides ; Integrin alphaXbeta2
Language	English
Publishing date	2024-02-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45627-y
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Article ; Online: Influenza A induces lactate formation to inhibit type I IFN in primary human airway epithelium.

Thyrsted, Jacob / Storgaard, Jacob / Blay-Cadanet, Julia / Heinz, Alexander / Thielke, Anne Laugaard / Crotta, Stefania / de Paoli, Frank / Olagnier, David / Wack, Andreas / Hiller, Karsten / Hansen, Anne Louise / Holm, Christian Kanstrup

iScience

2021 Volume 24, Issue 11, Page(s) 103300

Abstract: Pathogenic viruses induce metabolic changes in host cells to secure the availability of biomolecules and energy to propagate. Influenza A virus (IAV) and severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) both infect the human airway ... ...

Abstract	Pathogenic viruses induce metabolic changes in host cells to secure the availability of biomolecules and energy to propagate. Influenza A virus (IAV) and severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) both infect the human airway epithelium and are important human pathogens. The metabolic changes induced by these viruses in a physiologically relevant human model and how this affects innate immune responses to limit viral propagation are not well known. Using an ex vivo model of pseudostratified primary human airway epithelium, we here demonstrate that infection with both IAV and SARS-CoV-2 resulted in distinct metabolic changes including increases in lactate dehydrogenase A (LDHA) expression and LDHA-mediated lactate formation. Interestingly, LDHA regulated both basal and induced mitochondrial anti-viral signaling protein (MAVS)-dependent type I interferon (IFN) responses to promote IAV, but not SARS-CoV-2, replication. Our data demonstrate that LDHA and lactate promote IAV but not SARS-CoV-2 replication by inhibiting MAVS-dependent induction of type I IFN in primary human airway epithelium.
Language	English
Publishing date	2021-10-15
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103300
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Influenza A induces lactate formation to inhibit type I IFN in primary human airway epithelium

Jacob Thyrsted / Jacob Storgaard / Julia Blay-Cadanet / Alexander Heinz / Anne Laugaard Thielke / Stefania Crotta / Frank de Paoli / David Olagnier / Andreas Wack / Karsten Hiller / Anne Louise Hansen / Christian Kanstrup Holm

iScience, Vol 24, Iss 11, Pp 103300- (2021)

2021

Abstract: Summary: Pathogenic viruses induce metabolic changes in host cells to secure the availability of biomolecules and energy to propagate. Influenza A virus (IAV) and severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) both infect the human airway ... ...

Abstract	Summary: Pathogenic viruses induce metabolic changes in host cells to secure the availability of biomolecules and energy to propagate. Influenza A virus (IAV) and severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) both infect the human airway epithelium and are important human pathogens. The metabolic changes induced by these viruses in a physiologically relevant human model and how this affects innate immune responses to limit viral propagation are not well known. Using an ex vivo model of pseudostratified primary human airway epithelium, we here demonstrate that infection with both IAV and SARS-CoV-2 resulted in distinct metabolic changes including increases in lactate dehydrogenase A (LDHA) expression and LDHA-mediated lactate formation. Interestingly, LDHA regulated both basal and induced mitochondrial anti-viral signaling protein (MAVS)-dependent type I interferon (IFN) responses to promote IAV, but not SARS-CoV-2, replication. Our data demonstrate that LDHA and lactate promote IAV but not SARS-CoV-2 replication by inhibiting MAVS-dependent induction of type I IFN in primary human airway epithelium.
Keywords	Immune response ; Virology ; Metabolomics ; Science ; Q
Subject code	570
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Ionophore antibiotic X-206 is a potent inhibitor of SARS-CoV-2 infection in vitro.

Svenningsen, Esben B / Thyrsted, Jacob / Blay-Cadanet, Julia / Liu, Han / Lin, Shaoquan / Moyano-Villameriel, Jaime / Olagnier, David / Idorn, Manja / Paludan, Søren R / Holm, Christian K / Poulsen, Thomas B

Antiviral research

2020 Volume 185, Page(s) 104988

Abstract: Pandemic spread of emerging human pathogenic viruses, such as the current SARS-CoV-2, poses both an immediate and future challenge to human health and society. Currently, effective treatment of infection with SARS-CoV-2 is limited and broad spectrum ... ...

Abstract	Pandemic spread of emerging human pathogenic viruses, such as the current SARS-CoV-2, poses both an immediate and future challenge to human health and society. Currently, effective treatment of infection with SARS-CoV-2 is limited and broad spectrum antiviral therapies to meet other emerging pandemics are absent leaving the World population largely unprotected. Here, we have identified distinct members of the family of polyether ionophore antibiotics with potent ability to inhibit SARS-CoV-2 replication and cytopathogenicity in cells. Several compounds from this class displayed more than 100-fold selectivity between viral-induced cytopathogenicity and inhibition of cell viability, however the compound X-206 displayed >500-fold selectivity and was furthermore able to inhibit viral replication even at sub-nM levels. The antiviral mechanism of the polyether ionophores is currently not understood in detail. We demonstrate, e.g. through unbiased bioactivity profiling, that their effects on the host cells differ from those of cationic amphiphiles such as hydroxychloroquine. Collectively, our data suggest that polyether ionophore antibiotics should be subject to further investigations as potential broad-spectrum antiviral agents.
MeSH term(s)	Animals ; Anti-Bacterial Agents/pharmacology ; Antiviral Agents/pharmacology ; COVID-19/drug therapy ; Chlorocebus aethiops ; Ethers, Cyclic/pharmacology ; Humans ; Ionophores/pharmacology ; SARS-CoV-2/drug effects ; Vero Cells ; Virus Replication/drug effects
Chemical Substances	Anti-Bacterial Agents ; Antiviral Agents ; Ethers, Cyclic ; Ionophores ; X-206, polyether antibiotic
Language	English
Publishing date	2020-11-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2020.104988
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Zs.A 1627: Show issues

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Article ; Online: SARS-CoV-2 evades immune detection in alveolar macrophages.

Dalskov, Louise / Møhlenberg, Michelle / Thyrsted, Jacob / Blay-Cadanet, Julia / Poulsen, Ebbe Toftgaard / Folkersen, Birgitte Holst / Skaarup, Søren Helbo / Olagnier, David / Reinert, Line / Enghild, Jan Johannes / Hoffmann, Hans Jürgen / Holm, Christian Kanstrup / Hartmann, Rune

EMBO reports

2020 Volume 21, Issue 12, Page(s) e51252

Abstract: Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune ... ...

Abstract	Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS-CoV-2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non-infectious donors are challenged with SARS-CoV-2. We demonstrate that challenged AMs are incapable of sensing SARS-CoV-2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS-CoV-2 could explain the initial asymptotic phase observed during COVID-19 and argues against AMs being the sources of pro-inflammatory cytokines later during infection.
MeSH term(s)	Antiviral Agents/immunology ; COVID-19/immunology ; COVID-19/virology ; Cells, Cultured ; Cytokines/immunology ; Epithelial Cells/immunology ; Epithelial Cells/virology ; Humans ; Immune Evasion ; Interferon Type I/immunology ; Lung/immunology ; Lung/virology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/virology ; Pandemics ; SARS-CoV-2/immunology
Chemical Substances	Antiviral Agents ; Cytokines ; Interferon Type I
Keywords	covid19
Language	English
Publishing date	2020-10-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202051252
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Zs.A 5433: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 41: Show issues

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Article ; Online: TLR2 and TLR7 mediate distinct immunopathological and antiviral plasmacytoid dendritic cell responses to SARS-CoV-2 infection.

van der Sluis, Renée M / Cham, Lamin B / Gris-Oliver, Albert / Gammelgaard, Kristine R / Pedersen, Jesper G / Idorn, Manja / Ahmadov, Ulvi / Hernandez, Sabina Sanches / Cémalovic, Ena / Godsk, Stine H / Thyrsted, Jacob / Gunst, Jesper D / Nielsen, Silke D / Jørgensen, Janni J / Bjerg, Tobias Wang / Laustsen, Anders / Reinert, Line S / Olagnier, David / Bak, Rasmus O /

Kjolby, Mads / Holm, Christian K / Tolstrup, Martin / Paludan, Søren R / Kristensen, Lasse S / Søgaard, Ole S / Jakobsen, Martin R

The EMBO journal

2022 Volume 41, Issue 10, Page(s) e109622

Abstract: Understanding the molecular pathways driving the acute antiviral and inflammatory response to SARS-CoV-2 infection is critical for developing treatments for severe COVID-19. Here, we find decreasing number of circulating plasmacytoid dendritic cells ( ... ...

Abstract	Understanding the molecular pathways driving the acute antiviral and inflammatory response to SARS-CoV-2 infection is critical for developing treatments for severe COVID-19. Here, we find decreasing number of circulating plasmacytoid dendritic cells (pDCs) in COVID-19 patients early after symptom onset, correlating with disease severity. pDC depletion is transient and coincides with decreased expression of antiviral type I IFNα and of systemic inflammatory cytokines CXCL10 and IL-6. Using an in vitro stem cell-based human pDC model, we further demonstrate that pDCs, while not supporting SARS-CoV-2 replication, directly sense the virus and in response produce multiple antiviral (interferons: IFNα and IFNλ1) and inflammatory (IL-6, IL-8, CXCL10) cytokines that protect epithelial cells from de novo SARS-CoV-2 infection. Via targeted deletion of virus-recognition innate immune pathways, we identify TLR7-MyD88 signaling as crucial for production of antiviral interferons (IFNs), whereas Toll-like receptor (TLR)2 is responsible for the inflammatory IL-6 response. We further show that SARS-CoV-2 engages the receptor neuropilin-1 on pDCs to selectively mitigate the antiviral interferon response, but not the IL-6 response, suggesting neuropilin-1 as potential therapeutic target for stimulation of TLR7-mediated antiviral protection.
MeSH term(s)	COVID-19/immunology ; COVID-19/pathology ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Humans ; Interferon Type I/immunology ; Interferon-alpha/immunology ; Interleukin-6/immunology ; Neuropilin-1/immunology ; SARS-CoV-2 ; Toll-Like Receptor 2/immunology ; Toll-Like Receptor 7/immunology
Chemical Substances	Cytokines ; Interferon Type I ; Interferon-alpha ; Interleukin-6 ; TLR2 protein, human ; TLR7 protein, human ; Toll-Like Receptor 2 ; Toll-Like Receptor 7 ; Neuropilin-1 (144713-63-3)
Language	English
Publishing date	2022-03-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.2021109622
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Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 100: Show issues

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Article: SARS-CoV-2 evades immune detection in alveolar macrophages

EMBO Rep

Abstract	Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS-CoV-2 during an infection, and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non-infectious donors are challenged with SARS-CoV-2. We demonstrate that challenged AMs are incapable of sensing SARS-CoV-2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS-CoV-2 could explain the initial asymptotic phase observed during COVID-19 and argues against AMs being the sources of pro-inflammatory cytokines later during infection.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #895751
Database	COVID19

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