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Article ; Online: Competing Ligands Can Both Obstruct and Enhance Protein-Complex Formation.

Schreiber, Gideon

2019 Volume 117, Issue 9, Page(s) 1552–1553

MeSH term(s)	Cell Physiological Phenomena ; Ligands
Chemical Substances	Ligands
Language	English
Publishing date	2019-10-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2019.09.036
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Article ; Online: The Role of Type I Interferons in the Pathogenesis and Treatment of COVID-19.

Schreiber, Gideon

Frontiers in immunology

2020 Volume 11, Page(s) 595739

Abstract: Type I interferons (IFN-I) were first discovered over 60 years ago in a classical experiment by Isaacs and Lindenman, who showed that IFN-Is possess antiviral activity. Later, it became one of the first approved protein drugs using heterologous protein ... ...

Abstract	Type I interferons (IFN-I) were first discovered over 60 years ago in a classical experiment by Isaacs and Lindenman, who showed that IFN-Is possess antiviral activity. Later, it became one of the first approved protein drugs using heterologous protein expression systems, which allowed its large-scale production. It has been approved, and widely used in a pleiotropy of diseases, including multiple-sclerosis, hepatitis B and C, and some forms of cancer. Preliminary clinical data has supported its effectiveness against potential pandemic pathogens such as Ebola and SARS. Still, more efficient and specific drugs have taken its place in treating such diseases. The COVID-19 global pandemic has again lifted the status of IFN-Is to become one of the more promising drug candidates, with initial clinical trials showing promising results in reducing the severity and duration of the disease. Although SARS-CoV-2 inhibits the production of IFNβ and thus obstructs the innate immune response to this virus, it is sensitive to the antiviral activity of externally administrated IFN-Is. In this review I discuss the diverse modes of biological actions of IFN-Is and how these are related to biophysical parameters of IFN-I-receptor interaction and cell-type specificity in light of the large variety of binding affinities of the different IFN-I subtypes towards the common interferon receptor. Furthermore, I discuss how these may guide the optimized use IFN-Is in combatting COVID-19.
MeSH term(s)	Animals ; Antiviral Agents/therapeutic use ; Betacoronavirus/drug effects ; COVID-19 ; Clinical Trials as Topic ; Coronavirus Infections/drug therapy ; Coronavirus Infections/pathology ; Cytokine Release Syndrome/drug therapy ; Humans ; Immunity, Innate/drug effects ; Interferon Type I/therapeutic use ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/pathology ; SARS-CoV-2 ; Signal Transduction/immunology ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Interferon Type I
Keywords	covid19
Language	English
Publishing date	2020-09-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.595739
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Article ; Online: The Role of Type I Interferons in the Pathogenesis and Treatment of COVID-19

Gideon Schreiber

Frontiers in Immunology, Vol

2020 Volume 11

Abstract	Type I interferons (IFN-I) were first discovered over 60 years ago in a classical experiment by Isaacs and Lindenman, who showed that IFN-Is possess antiviral activity. Later, it became one of the first approved protein drugs using heterologous protein expression systems, which allowed its large-scale production. It has been approved, and widely used in a pleiotropy of diseases, including multiple-sclerosis, hepatitis B and C, and some forms of cancer. Preliminary clinical data has supported its effectiveness against potential pandemic pathogens such as Ebola and SARS. Still, more efficient and specific drugs have taken its place in treating such diseases. The COVID-19 global pandemic has again lifted the status of IFN-Is to become one of the more promising drug candidates, with initial clinical trials showing promising results in reducing the severity and duration of the disease. Although SARS-CoV-2 inhibits the production of IFNβ and thus obstructs the innate immune response to this virus, it is sensitive to the antiviral activity of externally administrated IFN-Is. In this review I discuss the diverse modes of biological actions of IFN-Is and how these are related to biophysical parameters of IFN-I–receptor interaction and cell-type specificity in light of the large variety of binding affinities of the different IFN-I subtypes towards the common interferon receptor. Furthermore, I discuss how these may guide the optimized use IFN-Is in combatting COVID-19.
Keywords	type I interferon ; COVID-19 ; signaling ; differential activity ; inflammation ; Immunologic diseases. Allergy ; RC581-607 ; covid19
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Role of Type I Interferons in the Pathogenesis and Treatment of COVID-19

Schreiber, Gideon

Frontiers in Immunology

2020 Volume 11

Keywords	covid19
Publisher	Frontiers Media SA
Publishing country	ch
Document type	Article ; Online
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.595739
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Article ; Online: Harnessing the power of IFN for therapeutic approaches to COVID-19.

Viox, Elise G / Bosinger, Steven E / Douek, Daniel C / Schreiber, Gideon / Paiardini, Mirko

Journal of virology

2024 , Page(s) e0120423

Abstract: Interferons (IFNs) are essential for defense against viral infections but also drive recruitment of inflammatory cells to sites of infection, a key feature of severe COVID-19. Here, we explore the complexity of the IFN response in COVID-19, examine the ... ...

Abstract	Interferons (IFNs) are essential for defense against viral infections but also drive recruitment of inflammatory cells to sites of infection, a key feature of severe COVID-19. Here, we explore the complexity of the IFN response in COVID-19, examine the effects of manipulating IFN on SARS-CoV-2 viral replication and pathogenesis, and highlight pre-clinical and clinical studies evaluating the therapeutic efficacy of IFN in limiting COVID-19 severity.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.01204-23
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Article: The Role of Type I Interferons in the Pathogenesis and Treatment of COVID-19

Schreiber, Gideon

Front Immunol

Abstract	Type I interferons (IFN-I) were first discovered over 60 years ago in a classical experiment by Isaacs and Lindenman, who showed that IFN-Is possess antiviral activity. Later, it became one of the first approved protein drugs using heterologous protein expression systems, which allowed its large-scale production. It has been approved, and widely used in a pleiotropy of diseases, including multiple-sclerosis, hepatitis B and C, and some forms of cancer. Preliminary clinical data has supported its effectiveness against potential pandemic pathogens such as Ebola and SARS. Still, more efficient and specific drugs have taken its place in treating such diseases. The COVID-19 global pandemic has again lifted the status of IFN-Is to become one of the more promising drug candidates, with initial clinical trials showing promising results in reducing the severity and duration of the disease. Although SARS-CoV-2 inhibits the production of IFNß and thus obstructs the innate immune response to this virus, it is sensitive to the antiviral activity of externally administrated IFN-Is. In this review I discuss the diverse modes of biological actions of IFN-Is and how these are related to biophysical parameters of IFN-I-receptor interaction and cell-type specificity in light of the large variety of binding affinities of the different IFN-I subtypes towards the common interferon receptor. Furthermore, I discuss how these may guide the optimized use IFN-Is in combatting COVID-19.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #886172
Database	COVID19

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Article ; Online: The molecular basis for differential type I interferon signaling.

Schreiber, Gideon

The Journal of biological chemistry

2017 Volume 292, Issue 18, Page(s) 7285–7294

Abstract: Type I interferons (IFN-1) are cytokines that affect the expression of thousands of genes, resulting in profound cellular changes. IFN-1 activates the cell by dimerizing its two-receptor chains, IFNAR1 and IFNAR2, which are expressed on all nucleated ... ...

Abstract	Type I interferons (IFN-1) are cytokines that affect the expression of thousands of genes, resulting in profound cellular changes. IFN-1 activates the cell by dimerizing its two-receptor chains, IFNAR1 and IFNAR2, which are expressed on all nucleated cells. Despite a similar mode of binding, the different IFN-1s activate a spectrum of activities. The causes for differential activation may stem from differences in IFN-1-binding affinity, duration of binding, number of surface receptors, induction of feedbacks, and cell type-specific variations. All together these will alter the signal that is transmitted from the extracellular domain inward. The intracellular domain binds, directly or indirectly, different effector proteins that transmit signals. The composition of effector molecules deviates between different cell types and tissues, inserting an additional level of complexity to the system. Moreover, IFN-1s do not act on their own, and clearly there is much cross-talk between the activated effector molecules by IFN-1 and other cytokines. The outcome generated by all of these factors (processing step) is an observed phenotype, which can be the transformation of the cell to an antiviral state, differentiation of the cell to a specific immune cell, senescence, apoptosis, and many more. IFN-1 activities can be divided into robust and tunable. Antiviral activity, which is stimulated by minute amounts of IFN-1 and is common to all cells, is termed robust. The other activities, which we term tunable, are cell type-specific and often require more stringent modes of activation. In this review, I summarize the current knowledge on the mode of activation and processing that is initiated by IFN-1, in perspective of the resulting phenotypes.
MeSH term(s)	Animals ; Humans ; Interferon-alpha/genetics ; Interferon-alpha/immunology ; Mice ; Phosphorylation/genetics ; Phosphorylation/immunology ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/immunology ; STAT Transcription Factors/genetics ; STAT Transcription Factors/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology
Chemical Substances	IFNAR1 protein, human ; IFNAR2 protein, human ; Ifnar1 protein, mouse ; Ifnar2 protein, mouse ; Interferon-alpha ; STAT Transcription Factors ; Receptor, Interferon alpha-beta (156986-95-7)
Language	English
Publishing date	2017-03-13
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.R116.774562
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Article ; Online: Enhanced transmissibility, infectivity, and immune resistance of the SARS-CoV-2 omicron XBB.1.5 variant.

Uriu, Keiya / Ito, Jumpei / Zahradnik, Jiri / Fujita, Shigeru / Kosugi, Yusuke / Schreiber, Gideon / Sato, Kei

The Lancet. Infectious diseases

2023 Volume 23, Issue 3, Page(s) 280–281

MeSH term(s)	Humans ; SARS-CoV-2 ; COVID-19
Language	English
Publishing date	2023-01-31
Publishing country	United States
Document type	Letter
ZDB-ID	2061641-7
ISSN	1474-4457 ; 1473-3099
ISSN (online)	1474-4457
ISSN	1473-3099
DOI	10.1016/S1473-3099(23)00051-8
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Article ; Online: Structure-function of type I and III interferons.

de Weerd, Nicole A / Kurowska, Aleksandra K / Mendoza, Juan L / Schreiber, Gideon

Current opinion in immunology

2024 Volume 86, Page(s) 102413

Abstract: Type I and type III interferons (IFNs) are major components in activating the innate immune response. Common to both are two distinct receptor chains (IFNAR1/IFNAR2 and IFNLR1/IL10R2), which form ternary complexes upon binding their respective ligands. ... ...

Abstract	Type I and type III interferons (IFNs) are major components in activating the innate immune response. Common to both are two distinct receptor chains (IFNAR1/IFNAR2 and IFNLR1/IL10R2), which form ternary complexes upon binding their respective ligands. This results in close proximity of the intracellularly associated kinases JAK1 and TYK2, which cross phosphorylate each other, the associated receptor chains, and signal transducer and activator of transcriptions, with the latter activating IFN-stimulated genes. While there are clear similarities in the biological responses toward type I and type III IFNs, differences have been found in their tropism, tuning of activity, and induction of the immune response. Here, we focus on how these differences are embedded in the structure/function relations of these two systems in light of the recent progress that provides in-depth information on the structural assembly of these receptors and their functional implications and how these differ between the mouse and human systems.
MeSH term(s)	Humans ; Animals ; Mice ; Interferons ; Receptors, Interferon/metabolism ; Receptor, Interferon alpha-beta/genetics ; Signal Transduction/genetics ; Immunity, Innate ; Interferon Type I/metabolism
Chemical Substances	Interferons (9008-11-1) ; Receptors, Interferon ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferon Type I ; IFNLR1 protein, mouse
Language	English
Publishing date	2024-04-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2024.102413
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Article ; Online: Protein Engineering in the Design of Protein-Protein Interactions: SARS-CoV-2 Inhibitors as a Test Case.

Zahradník, Jiří / Schreiber, Gideon

Biochemistry

2021 Volume 60, Issue 46, Page(s) 3429–3435

Abstract: The formation of specific protein-protein interactions (PPIs) drive most biological processes. Malfunction of such interactions is the molecular driver of many diseases. Our ability to engineer existing PPIs or create new ones has become a vital research ...

Abstract	The formation of specific protein-protein interactions (PPIs) drive most biological processes. Malfunction of such interactions is the molecular driver of many diseases. Our ability to engineer existing PPIs or create new ones has become a vital research tool. In addition, engineered proteins with new or altered interactions are among the most critical drugs that have been developed in recent years. These include antibodies, cytokines, inhibitors, and others. Here, we provide a perspective on the current status of the methods used to engineer new or altered PPIs. The emergence of the COVID-19 pandemic, which resulted in a worldwide quest to develop specific PPI inhibitors as drugs, provided an up-to-date and state-of-the-art status report on the methodologies for engineering PPIs targeting the interaction of the viral spike protein with its cellular target, ACE2. Multiple, very high affinity binders were generated within a few months using
MeSH term(s)	Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; Antibodies, Neutralizing/metabolism ; Antibodies, Viral/metabolism ; Antiviral Agents/therapeutic use ; COVID-19/metabolism ; COVID-19/prevention & control ; COVID-19/virology ; Computational Biology ; Humans ; Protein Binding ; Protein Engineering/methods ; Protein Interaction Domains and Motifs ; SARS-CoV-2/metabolism ; Spike Glycoprotein, Coronavirus/genetics ; Spike Glycoprotein, Coronavirus/metabolism
Chemical Substances	Antibodies, Neutralizing ; Antibodies, Viral ; Antiviral Agents ; Spike Glycoprotein, Coronavirus ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108-3
ISSN	1520-4995 ; 0006-2960
ISSN (online)	1520-4995
ISSN	0006-2960
DOI	10.1021/acs.biochem.1c00356
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