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  1. Article ; Online: Sarbecovirus ORF6 proteins hamper induction of interferon signaling.

    Kimura, Izumi / Konno, Yoriyuki / Uriu, Keiya / Hopfensperger, Kristina / Sauter, Daniel / Nakagawa, So / Sato, Kei

    Cell reports

    2021  Volume 34, Issue 13, Page(s) 108916

    Abstract: The presence of an ORF6 gene distinguishes sarbecoviruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 from other betacoronaviruses. Here we show that ORF6 inhibits induction of innate immune signaling, including ... ...

    Abstract The presence of an ORF6 gene distinguishes sarbecoviruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 from other betacoronaviruses. Here we show that ORF6 inhibits induction of innate immune signaling, including upregulation of type I interferon (IFN) upon viral infection as well as type I and III IFN signaling. Intriguingly, ORF6 proteins from SARS-CoV-2 lineages are more efficient antagonists of innate immunity than their orthologs from SARS-CoV lineages. Mutational analyses identified residues E46 and Q56 as important determinants of the antagonistic activity of SARS-CoV-2 ORF6. Moreover, we show that the anti-innate immune activity of ORF6 depends on its C-terminal region and that ORF6 inhibits nuclear translocation of IRF3. Finally, we identify naturally occurring frameshift/nonsense mutations that result in an inactivating truncation of ORF6 in approximately 0.2% of SARS-CoV-2 isolates. Our findings suggest that ORF6 contributes to the poor IFN activation observed in individuals with coronavirus disease 2019 (COVID-19).
    MeSH term(s) Animals ; COVID-19/genetics ; COVID-19/metabolism ; Chlorocebus aethiops ; HEK293 Cells ; Humans ; Immunity, Innate/immunology ; Interferon Type I/metabolism ; SARS-CoV-2/isolation & purification ; Signal Transduction/immunology ; Vero Cells ; Viral Proteins/genetics ; Viral Proteins/metabolism
    Chemical Substances Interferon Type I ; ORF6 protein, SARS-CoV-2 ; Viral Proteins
    Language English
    Publishing date 2021-03-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.108916
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sarbecovirus ORF6 proteins hamper induction of interferon signaling

    Izumi Kimura / Yoriyuki Konno / Keiya Uriu / Kristina Hopfensperger / Daniel Sauter / So Nakagawa / Kei Sato

    Cell Reports, Vol 34, Iss 13, Pp 108916- (2021)

    2021  

    Abstract: Summary: The presence of an ORF6 gene distinguishes sarbecoviruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 from other betacoronaviruses. Here we show that ORF6 inhibits induction of innate immune signaling, ... ...

    Abstract Summary: The presence of an ORF6 gene distinguishes sarbecoviruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 from other betacoronaviruses. Here we show that ORF6 inhibits induction of innate immune signaling, including upregulation of type I interferon (IFN) upon viral infection as well as type I and III IFN signaling. Intriguingly, ORF6 proteins from SARS-CoV-2 lineages are more efficient antagonists of innate immunity than their orthologs from SARS-CoV lineages. Mutational analyses identified residues E46 and Q56 as important determinants of the antagonistic activity of SARS-CoV-2 ORF6. Moreover, we show that the anti-innate immune activity of ORF6 depends on its C-terminal region and that ORF6 inhibits nuclear translocation of IRF3. Finally, we identify naturally occurring frameshift/nonsense mutations that result in an inactivating truncation of ORF6 in approximately 0.2% of SARS-CoV-2 isolates. Our findings suggest that ORF6 contributes to the poor IFN activation observed in individuals with coronavirus disease 2019 (COVID-19).
    Keywords SARS-CoV-2 ; COVID-19 ; ORF6 ; type I interferon ; type III interferon ; interferon-stimulated gene ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
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  3. Article ; Online: Two-step evolution of HIV-1 budding system leading to pandemic in the human population.

    Konno, Yoriyuki / Uriu, Keiya / Chikata, Takayuki / Takada, Toru / Kurita, Jun-Ichi / Ueda, Mahoko Takahashi / Islam, Saiful / Yang Tan, Benjy Jek / Ito, Jumpei / Aso, Hirofumi / Kumata, Ryuichi / Williamson, Carolyn / Iwami, Shingo / Takiguchi, Masafumi / Nishimura, Yoshifumi / Morita, Eiji / Satou, Yorifumi / Nakagawa, So / Koyanagi, Yoshio /
    Sato, Kei

    Cell reports

    2024  Volume 43, Issue 2, Page(s) 113697

    Abstract: The pandemic HIV-1, HIV-1 group M, emerged from a single spillover event of its ancestral lentivirus from a chimpanzee. During human-to-human spread worldwide, HIV-1 diversified into multiple subtypes. Here, our interdisciplinary investigation mainly ... ...

    Abstract The pandemic HIV-1, HIV-1 group M, emerged from a single spillover event of its ancestral lentivirus from a chimpanzee. During human-to-human spread worldwide, HIV-1 diversified into multiple subtypes. Here, our interdisciplinary investigation mainly sheds light on the evolutionary scenario of the viral budding system of HIV-1 subtype C (HIV-1C), a most successfully spread subtype. Of the two amino acid motifs for HIV-1 budding, the P(T/S)AP and YPxL motifs, HIV-1C loses the YPxL motif. Our data imply that HIV-1C might lose this motif to evade immune pressure. Additionally, the P(T/S)AP motif is duplicated dependently of the level of HIV-1 spread in the human population, and >20% of HIV-1C harbored the duplicated P(T/S)AP motif. We further show that the duplication of the P(T/S)AP motif is caused by the expansion of the CTG triplet repeat. Altogether, our results suggest that HIV-1 has experienced a two-step evolution of the viral budding process during human-to-human spread worldwide.
    MeSH term(s) Humans ; Animals ; HIV-1/genetics ; Pandemics ; Lentivirus ; Cell Division ; HIV Seropositivity ; Pan troglodytes
    Language English
    Publishing date 2024-01-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.113697
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Comprehensive Investigation on the Interplay between Feline APOBEC3Z3 Proteins and Feline Immunodeficiency Virus Vif Proteins.

    Kosugi, Yusuke / Uriu, Keiya / Suzuki, Narumi / Yamamoto, Keisuke / Nagaoka, Shumpei / Kimura, Izumi / Konno, Yoriyuki / Aso, Hirofumi / Willett, Brian J / Kobayashi, Tomoko / Koyanagi, Yoshio / Ueda, Mahoko Takahashi / Ito, Jumpei / Sato, Kei

    Journal of virology

    2021  Volume 95, Issue 13, Page(s) e0017821

    Abstract: As the hosts of lentiviruses, almost 40 species of felids ( ... ...

    Abstract As the hosts of lentiviruses, almost 40 species of felids (family
    MeSH term(s) APOBEC-1 Deaminase/metabolism ; Animals ; Cats ; Cell Line ; Gene Products, vif/metabolism ; HEK293 Cells ; Host Specificity/physiology ; Host-Pathogen Interactions/physiology ; Humans ; Immunodeficiency Virus, Feline/metabolism ; Lentivirus Infections/pathology ; Lentivirus Infections/transmission ; Panthera ; Virus Replication/physiology
    Chemical Substances Gene Products, vif ; APOBEC-1 Deaminase (EC 3.5.4.36)
    Language English
    Publishing date 2021-06-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00178-21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 609: 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)

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  5. Article: Type I Interferon Responses by HIV-1 Infection: Association with Disease Progression and Control.

    Soper, Andrew / Kimura, Izumi / Nagaoka, Shumpei / Konno, Yoriyuki / Yamamoto, Keisuke / Koyanagi, Yoshio / Sato, Kei

    Frontiers in immunology

    2017  Volume 8, Page(s) 1823

    Abstract: Human immunodeficiency virus type 1 (HIV-1) is the causative agent of acquired immunodeficiency syndrome and its infection leads to the onset of several disorders such as the depletion of peripheral ... ...

    Abstract Human immunodeficiency virus type 1 (HIV-1) is the causative agent of acquired immunodeficiency syndrome and its infection leads to the onset of several disorders such as the depletion of peripheral CD4
    Language English
    Publishing date 2017
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2017.01823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: SARS-CoV-2 ORF3b Is a Potent Interferon Antagonist Whose Activity Is Increased by a Naturally Occurring Elongation Variant.

    Konno, Yoriyuki / Kimura, Izumi / Uriu, Keiya / Fukushi, Masaya / Irie, Takashi / Koyanagi, Yoshio / Sauter, Daniel / Gifford, Robert J / Nakagawa, So / Sato, Kei

    Cell reports

    2020  Volume 32, Issue 12, Page(s) 108185

    Abstract: One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of ... ...

    Abstract One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of type I interferon more efficiently than its SARS-CoV ortholog. Phylogenetic analyses and functional assays reveal that SARS-CoV-2-related viruses from bats and pangolins also encode truncated ORF3b gene products with strong anti-interferon activity. Furthermore, analyses of approximately 17,000 SARS-CoV-2 sequences identify a natural variant in which a longer ORF3b reading frame was reconstituted. This variant was isolated from two patients with severe disease and further increased the ability of ORF3b to suppress interferon induction. Thus, our findings not only help to explain the poor interferon response in COVID-19 patients but also describe the emergence of natural SARS-CoV-2 quasispecies with an extended ORF3b gene that may potentially affect COVID-19 pathogenesis.
    MeSH term(s) Adult ; Amino Acid Sequence/genetics ; Animals ; Betacoronavirus/genetics ; Betacoronavirus/immunology ; COVID-19 ; Chiroptera/virology ; Codon, Nonsense/genetics ; Coronavirus Infections/pathology ; Coronavirus Infections/virology ; Eutheria/virology ; Humans ; Interferon Type I/antagonists & inhibitors ; Male ; Pandemics ; Pneumonia, Viral/virology ; SARS-CoV-2 ; Viral Regulatory and Accessory Proteins/genetics ; Viral Regulatory and Accessory Proteins/metabolism
    Chemical Substances Codon, Nonsense ; Interferon Type I ; Viral Regulatory and Accessory Proteins
    Keywords covid19
    Language English
    Publishing date 2020-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2020.108185
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  7. Article ; Online: A naturally occurring feline APOBEC3 variant that loses anti-lentiviral activity by lacking two amino acid residues.

    Konno, Yoriyuki / Nagaoka, Shumpei / Kimura, Izumi / Takahashi Ueda, Mahoko / Kumata, Ryuichi / Ito, Jumpei / Nakagawa, So / Kobayashi, Tomoko / Koyanagi, Yoshio / Sato, Kei

    The Journal of general virology

    2018  Volume 99, Issue 5, Page(s) 704–709

    Abstract: Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) is a mammalian protein that restricts lentiviral replication. Various polymorphisms of ... ...

    Abstract Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) is a mammalian protein that restricts lentiviral replication. Various polymorphisms of mammalian
    Language English
    Publishing date 2018-04-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 219316-4
    ISSN 1465-2099 ; 0022-1317
    ISSN (online) 1465-2099
    ISSN 0022-1317
    DOI 10.1099/jgv.0.001046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 610: 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)

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  8. Article ; Online: SARS-CoV-2 ORF3b is a potent interferon antagonist whose activity is further increased by a naturally occurring elongation variant

    Konno, Yoriyuki / Kimura, Izumi / Uriu, Keiya / Fukushi, Masaya / Irie, Takashi / Koyanagi, Yoshio / Nakagawa, So / Sato, Kei

    bioRxiv

    Abstract: One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of ... ...

    Abstract One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of type I interferon more efficiently than its SARS-CoV ortholog. Phylogenetic analyses and functional assays revealed that SARS-CoV-2-related viruses from bats and pangolins also encode truncated ORF3b gene products with strong anti-interferon activity. Furthermore, analyses of more than 15,000 SARS-CoV-2 sequences identified a natural variant, in which a longer ORF3b reading frame was reconstituted. This variant was isolated from two patients with severe disease and further increased the ability of ORF3b to suppress interferon induction. Thus, our findings not only help to explain the poor interferon response in COVID-19 patients, but also describe a possibility of the emergence of natural SARS-CoV-2 quasispecies with extended ORF3b that may exacerbate COVID-19 symptoms.
    Keywords covid19
    Language English
    Publishing date 2020-05-12
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2020.05.11.088179
    Database COVID19

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  9. Article ; Online: SARS-CoV-2 ORF3b Is a Potent Interferon Antagonist Whose Activity Is Increased by a Naturally Occurring Elongation Variant

    Yoriyuki Konno / Izumi Kimura / Keiya Uriu / Masaya Fukushi / Takashi Irie / Yoshio Koyanagi / Daniel Sauter / Robert J. Gifford / So Nakagawa / Kei Sato

    Cell Reports, Vol 32, Iss 12, Pp 108185- (2020)

    2020  

    Abstract: Summary: One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the ... ...

    Abstract Summary: One of the features distinguishing SARS-CoV-2 from its more pathogenic counterpart SARS-CoV is the presence of premature stop codons in its ORF3b gene. Here, we show that SARS-CoV-2 ORF3b is a potent interferon antagonist, suppressing the induction of type I interferon more efficiently than its SARS-CoV ortholog. Phylogenetic analyses and functional assays reveal that SARS-CoV-2-related viruses from bats and pangolins also encode truncated ORF3b gene products with strong anti-interferon activity. Furthermore, analyses of approximately 17,000 SARS-CoV-2 sequences identify a natural variant in which a longer ORF3b reading frame was reconstituted. This variant was isolated from two patients with severe disease and further increased the ability of ORF3b to suppress interferon induction. Thus, our findings not only help to explain the poor interferon response in COVID-19 patients but also describe the emergence of natural SARS-CoV-2 quasispecies with an extended ORF3b gene that may potentially affect COVID-19 pathogenesis.
    Keywords SARS-CoV-2 ; COVID-19 ; ORF3b ; type I interferon ; evolution ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  10. Article ; Online: SARS-CoV-2 ORF3b Is a Potent Interferon Antagonist Whose Activity Is Increased by a Naturally Occurring Elongation Variant

    Konno, Yoriyuki / Kimura, Izumi / Uriu, Keiya / Fukushi, Masaya / Irie, Takashi / Koyanagi, Yoshio / Sauter, Daniel / Gifford, Robert J. / Nakagawa, So / Sato, Kei

    Cell Reports

    2020  Volume 32, Issue 12, Page(s) 108185

    Keywords General Biochemistry, Genetics and Molecular Biology ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2649101-1
    ISSN 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2020.108185
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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