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  1. Article ; Online: Omicron variant of SARS-CoV-2 exhibits an increased resilience to the antiviral type I interferon response.

    Shalamova, Lyudmila / Felgenhauer, Ulrike / Wilhelm, Jochen / Schaubmar, Andreas R / Büttner, Kathrin / Schoen, Andreas / Widera, Marek / Ciesek, Sandra / Weber, Friedemann

    PNAS nexus

    2022  Volume 1, Issue 2, Page(s) pgac067

    Abstract: The new variant of concern (VOC) of SARS-CoV-2, Omicron (B.1.1.529), is genetically very different from other VOCs. We compared Omicron with the preceding VOC Delta (B.1.617.2) and the wildtype (wt) strain (B.1) with respect to their interactions with ... ...

    Abstract The new variant of concern (VOC) of SARS-CoV-2, Omicron (B.1.1.529), is genetically very different from other VOCs. We compared Omicron with the preceding VOC Delta (B.1.617.2) and the wildtype (wt) strain (B.1) with respect to their interactions with the antiviral interferon (IFN-alpha/beta) response in infected cells. Our data indicate that IFN induction by Omicron is low and comparable to the wt, whereas Delta showed an increased IFN induction. However, Omicron exceeded both the wt and the Delta strain with respect to the ability to withstand the antiviral state imposed by IFN-alpha.
    Language English
    Publishing date 2022-05-23
    Publishing country England
    Document type Journal Article
    ISSN 2752-6542
    ISSN (online) 2752-6542
    DOI 10.1093/pnasnexus/pgac067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Omicron variant of SARS-CoV-2 exhibits an increased resilience to the antiviral type I interferon response

    Shalamova, Lyudmila / Felgenhauer, Ulrike / Schaubmar, Andreas R. / Buettner, Kathrin / Widera, Marek / Ciesek, Sandra / Weber, Friedemann

    bioRxiv

    Abstract: The new variant of concern (VOC) of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Omicron (B.1.1.529), is genetically very different from other VOCs. We compared Omicron with the preceding VOC Delta (B.1.617.2) and the wildtype strain ...

    Abstract The new variant of concern (VOC) of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Omicron (B.1.1.529), is genetically very different from other VOCs. We compared Omicron with the preceding VOC Delta (B.1.617.2) and the wildtype strain (B.1) with respect to their interactions with the antiviral type I interferon (IFN-alpha/beta) response in infected cells. Our data indicate that Omicron has gained an elevated capability to suppress IFN induction upon infection and to better withstand the antiviral state imposed by exogenously added IFN-alpha.
    Keywords covid19
    Language English
    Publishing date 2022-01-20
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2022.01.20.476754
    Database COVID19

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  3. Article ; Online: Inhibition of SARS-CoV-2 by type I and type III interferons.

    Felgenhauer, Ulrike / Schoen, Andreas / Gad, Hans Henrik / Hartmann, Rune / Schaubmar, Andreas R / Failing, Klaus / Drosten, Christian / Weber, Friedemann

    The Journal of biological chemistry

    2020  Volume 295, Issue 41, Page(s) 13958–13964

    Abstract: The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-α) and type ... ...

    Abstract The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-α) and type III (IFN-λ) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-α in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.
    MeSH term(s) Animals ; Antiviral Agents/pharmacology ; Betacoronavirus/drug effects ; Betacoronavirus/isolation & purification ; Betacoronavirus/physiology ; COVID-19 ; Cell Line ; Chlorocebus aethiops ; Coronavirus Infections/pathology ; Coronavirus Infections/virology ; Humans ; Interferon Type I/pharmacology ; Interferons/pharmacology ; Janus Kinases/metabolism ; Nitriles ; Pandemics ; Pneumonia, Viral/pathology ; Pneumonia, Viral/virology ; Pyrazoles/pharmacology ; Pyrimidines ; Severe acute respiratory syndrome-related coronavirus/drug effects ; Severe acute respiratory syndrome-related coronavirus/physiology ; SARS-CoV-2 ; Signal Transduction/drug effects ; Vero Cells ; Virus Replication/drug effects ; Interferon Lambda
    Chemical Substances Antiviral Agents ; Interferon Type I ; Nitriles ; Pyrazoles ; Pyrimidines ; ruxolitinib (82S8X8XX8H) ; Interferons (9008-11-1) ; Janus Kinases (EC 2.7.10.2) ; Interferon Lambda
    Keywords covid19
    Language English
    Publishing date 2020-06-25
    Publishing country United States
    Document type Journal Article ; 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.AC120.013788
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Identification of SARS-CoV-2-induced pathways reveals drug repurposing strategies.

    Han, Namshik / Hwang, Woochang / Tzelepis, Konstantinos / Schmerer, Patrick / Yankova, Eliza / MacMahon, Méabh / Lei, Winnie / M Katritsis, Nicholas / Liu, Anika / Felgenhauer, Ulrike / Schuldt, Alison / Harris, Rebecca / Chapman, Kathryn / McCaughan, Frank / Weber, Friedemann / Kouzarides, Tony

    Science advances

    2021  Volume 7, Issue 27

    Abstract: The global outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) necessitates the rapid development of new therapies against coronavirus disease 2019 (COVID-19) infection. Here, we present the identification of 200 approved drugs, ... ...

    Abstract The global outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) necessitates the rapid development of new therapies against coronavirus disease 2019 (COVID-19) infection. Here, we present the identification of 200 approved drugs, appropriate for repurposing against COVID-19. We constructed a SARS-CoV-2-induced protein network, based on disease signatures defined by COVID-19 multiomics datasets, and cross-examined these pathways against approved drugs. This analysis identified 200 drugs predicted to target SARS-CoV-2-induced pathways, 40 of which are already in COVID-19 clinical trials, testifying to the validity of the approach. Using artificial neural network analysis, we classified these 200 drugs into nine distinct pathways, within two overarching mechanisms of action (MoAs): viral replication (126) and immune response (74). Two drugs (proguanil and sulfasalazine) implicated in viral replication were shown to inhibit replication in cell assays. This unbiased and validated analysis opens new avenues for the rapid repurposing of approved drugs into clinical trials.
    MeSH term(s) Antiviral Agents/metabolism ; Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; COVID-19/pathology ; COVID-19/virology ; Drug Repositioning ; Humans ; Neural Networks, Computer ; Proguanil/pharmacology ; Proguanil/therapeutic use ; SARS-CoV-2/immunology ; SARS-CoV-2/isolation & purification ; SARS-CoV-2/physiology ; Sulfasalazine/pharmacology ; Virus Replication/drug effects ; COVID-19 Drug Treatment
    Chemical Substances Antiviral Agents ; Sulfasalazine (3XC8GUZ6CB) ; Proguanil (S61K3P7B2V)
    Language English
    Publishing date 2021-06-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abh3032
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Inhibition of SARS-CoV-2 by type I and type III interferons

    Felgenhauer, Ulrike / Schoen, Andreas / Gad, Hans Henrik / Hartmann, Rune / Schaubmar, Andreas R / Failing, Klaus / Drosten, Christian / Weber, Friedemann

    J. biol. chem

    Abstract: The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-alpha) and ... ...

    Abstract The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-alpha in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #32587093
    Database COVID19

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  6. Article ; Online: Inhibition of SARS-CoV-2 by type I and type III interferons

    Felgenhauer, Ulrike / Schoen, Andreas / Gad, Hans Henrik / Hartmann, Rune / Schaubmar, Andreas R / Failing, Klaus / Drosten, Christian / Weber, Friedemann

    Felgenhauer , U , Schoen , A , Gad , H H , Hartmann , R , Schaubmar , A R , Failing , K , Drosten , C & Weber , F 2020 , ' Inhibition of SARS-CoV-2 by type I and type III interferons ' , The Journal of Biological Chemistry , vol. 295 , no. 41 . https://doi.org/10.1074/jbc.AC120.013788

    2020  

    Abstract: The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-α) and type ... ...

    Abstract The recently emerged severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of the devastating COVID-19 lung disease pandemic. Here, we tested the inhibitory activities of the antiviral interferons of type I (IFN-α) and type III (IFN-λ) against SARS-CoV-2 and compared them with those against SARS-CoV-1, which emerged in 2003. Using two mammalian epithelial cell lines (human Calu-3 and simian Vero E6), we found that both IFNs dose-dependently inhibit SARS-CoV-2. In contrast, SARS-CoV-1 was restricted only by IFN-α in these cell lines. SARS-CoV-2 generally exhibited a broader IFN sensitivity than SARS-CoV-1. Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells. We conclude that SARS-CoV-2 is sensitive to exogenously added IFNs. This finding suggests that type I and especially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.
    Keywords covid19
    Language English
    Publishing country dk
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Influenza virus adaptation PB2-627K modulates nucleocapsid inhibition by the pathogen sensor RIG-I.

    Weber, Michaela / Sediri, Hanna / Felgenhauer, Ulrike / Binzen, Ina / Bänfer, Sebastian / Jacob, Ralf / Brunotte, Linda / García-Sastre, Adolfo / Schmid-Burgk, Jonathan L / Schmidt, Tobias / Hornung, Veit / Kochs, Georg / Schwemmle, Martin / Klenk, Hans-Dieter / Weber, Friedemann

    Cell host & microbe

    2015  Volume 17, Issue 3, Page(s) 309–319

    Abstract: The cytoplasmic RNA helicase RIG-I mediates innate sensing of RNA viruses. The genomes of influenza A virus (FLUAV) are encapsidated by the nucleoprotein and associated with RNA polymerase, posing potential barriers to RIG-I sensing. We show that RIG-I ... ...

    Abstract The cytoplasmic RNA helicase RIG-I mediates innate sensing of RNA viruses. The genomes of influenza A virus (FLUAV) are encapsidated by the nucleoprotein and associated with RNA polymerase, posing potential barriers to RIG-I sensing. We show that RIG-I recognizes the 5'-triphosphorylated dsRNA on FLUAV nucleocapsids but that polymorphisms at position 627 of the viral polymerase subunit PB2 modulate RIG-I sensing. Compared to mammalian-adapted PB2-627K, avian FLUAV nucleocapsids possessing PB2-627E are prone to increased RIG-I recognition, and RIG-I-deficiency partially restores PB2-627E virus infection of mammalian cells. Heightened RIG-I sensing of PB2-627E nucleocapsids correlates with previously established lower affinity of 627E-containing PB2 for nucleoprotein and is increased by further nucleocapsid instability. The effect of RIG-I on PB2-627E nucleocapsids is independent of antiviral signaling, suggesting that RIG-I-nucleocapsid binding alone can inhibit infection. These results indicate that RIG-I is a direct avian FLUAV restriction factor and highlight nucleocapsid disruption as an antiviral strategy.
    MeSH term(s) Animals ; Cell Line ; DEAD Box Protein 58 ; DEAD-box RNA Helicases/metabolism ; Host-Pathogen Interactions ; Humans ; Influenza A virus/genetics ; Influenza A virus/immunology ; Influenza A virus/physiology ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Nucleocapsid/genetics ; Nucleocapsid/immunology ; Nucleocapsid/physiology ; Orthomyxoviridae ; Protein Binding ; RNA, Double-Stranded/metabolism ; RNA, Viral/metabolism ; RNA-Dependent RNA Polymerase/genetics ; RNA-Dependent RNA Polymerase/metabolism ; Receptors, Immunologic ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Replication
    Chemical Substances Mutant Proteins ; PB2 protein, Influenzavirus A ; RNA, Double-Stranded ; RNA, Viral ; Receptors, Immunologic ; Viral Proteins ; RNA-Dependent RNA Polymerase (EC 2.7.7.48) ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2015-02-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2278004-X
    ISSN 1934-6069 ; 1931-3128
    ISSN (online) 1934-6069
    ISSN 1931-3128
    DOI 10.1016/j.chom.2015.01.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6578: Show issues Location:
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