SrasV1, Ncbi, Merge, bibRecord, 002C74

Infectious Bronchitis Coronavirus Limits Interferon Production by Inducing a Host Shutoff That Requires Accessory Protein 5b.

Identifieur interne : 002C74 ( Ncbi/Merge ); précédent : 002C73; suivant : 002C75

Infectious Bronchitis Coronavirus Limits Interferon Production by Inducing a Host Shutoff That Requires Accessory Protein 5b.

Auteurs : Joeri Kint [Pays-Bas] ; Martijn A. Langereis [Pays-Bas] ; Helena J. Maier [Royaume-Uni] ; Paul Britton [Royaume-Uni] ; Frank J. Van Kuppeveld [Pays-Bas] ; Joseph Koumans [Pays-Bas] ; Geert F. Wiegertjes [Pays-Bas] ; Maria Forlenza [Pays-Bas]

Source :

Journal of virology [ 1098-5514 ] ; 2016.

RBID : pubmed:27279618

Descripteurs français

KwdFr :
- Animaux, Cellules cultivées, Interactions hôte-pathogène, Interféron de type I (antagonistes et inhibiteurs), Poulets, Protéines virales (génétique), Protéines virales (métabolisme), Techniques de knock-out de gènes, Virus de la bronchite infectieuse (génétique), Virus de la bronchite infectieuse (immunologie), Virus de la bronchite infectieuse (pathogénicité), Échappement immunitaire.
MESH :
- antagonistes et inhibiteurs : Interféron de type I.
- génétique : Protéines virales, Virus de la bronchite infectieuse.
- immunologie : Virus de la bronchite infectieuse.
- métabolisme : Protéines virales.
- pathogénicité : Virus de la bronchite infectieuse.
- Animaux, Cellules cultivées, Interactions hôte-pathogène, Poulets, Techniques de knock-out de gènes, Échappement immunitaire.

English descriptors

KwdEn :
- Animals, Cells, Cultured, Chickens, Gene Knockout Techniques, Host-Pathogen Interactions, Immune Evasion, Infectious bronchitis virus (genetics), Infectious bronchitis virus (immunology), Infectious bronchitis virus (pathogenicity), Interferon Type I (antagonists & inhibitors), Viral Proteins (genetics), Viral Proteins (metabolism).
MESH :
- chemical , antagonists & inhibitors : Interferon Type I.
- genetics : Infectious bronchitis virus, Viral Proteins.
- immunology : Infectious bronchitis virus.
- chemical , metabolism : Viral Proteins.
- pathogenicity : Infectious bronchitis virus.
- Animals, Cells, Cultured, Chickens, Gene Knockout Techniques, Host-Pathogen Interactions, Immune Evasion.

Abstract

During infection of their host cells, viruses often inhibit the production of host proteins, a process that is referred to as host shutoff. By doing this, viruses limit the production of antiviral proteins and increase production capacity for viral proteins. Coronaviruses from the genera Alphacoronavirus and Betacoronavirus, such as severe acute respiratory syndrome coronavirus (SARS-CoV), establish host shutoff via their nonstructural protein 1 (nsp1). The Gammacoronavirus and Deltacoronavirus genomes, however, do not encode nsp1, and it has been suggested that these viruses do not induce host shutoff. Here, we show that the Gammacoronavirus infectious bronchitis virus (IBV) does induce host shutoff, and we find that its accessory protein 5b is indispensable for this function. Importantly, we found that 5b-null viruses, unlike wild-type viruses, induce production of high concentrations of type I interferon protein in vitro, indicating that host shutoff by IBV plays an important role in antagonizing the host's innate immune response. Altogether, we demonstrate that 5b is a functional equivalent of nsp1, thereby answering the longstanding question of whether lack of nsp1 in gammacoronaviruses is compensated for by another viral protein. As such, our study is a significant step forward in the understanding of coronavirus biology and closes a gap in the understanding of some IBV virulence strategies.

DOI: 10.1128/JVI.00627-16
PubMed: 27279618

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to stream PubMed, to step Corpus: 000C40
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Le document en format XML

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<term>Host-Pathogen Interactions</term>
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<term>Infectious bronchitis virus (immunology)</term>
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<term>Virus de la bronchite infectieuse (pathogénicité)</term>
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<front><div type="abstract" xml:lang="en">During infection of their host cells, viruses often inhibit the production of host proteins, a process that is referred to as host shutoff. By doing this, viruses limit the production of antiviral proteins and increase production capacity for viral proteins. Coronaviruses from the genera Alphacoronavirus and Betacoronavirus, such as severe acute respiratory syndrome coronavirus (SARS-CoV), establish host shutoff via their nonstructural protein 1 (nsp1). The Gammacoronavirus and Deltacoronavirus genomes, however, do not encode nsp1, and it has been suggested that these viruses do not induce host shutoff. Here, we show that the Gammacoronavirus infectious bronchitis virus (IBV) does induce host shutoff, and we find that its accessory protein 5b is indispensable for this function. Importantly, we found that 5b-null viruses, unlike wild-type viruses, induce production of high concentrations of type I interferon protein in vitro, indicating that host shutoff by IBV plays an important role in antagonizing the host's innate immune response. Altogether, we demonstrate that 5b is a functional equivalent of nsp1, thereby answering the longstanding question of whether lack of nsp1 in gammacoronaviruses is compensated for by another viral protein. As such, our study is a significant step forward in the understanding of coronavirus biology and closes a gap in the understanding of some IBV virulence strategies.</div>
</front>
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<DateCompleted><Year>2017</Year>
<Month>05</Month>
<Day>08</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>90</Volume>
<Issue>16</Issue>
<PubDate><Year>2016</Year>
<Month>08</Month>
<Day>15</Day>
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<Title>Journal of virology</Title>
<ISOAbbreviation>J. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Infectious Bronchitis Coronavirus Limits Interferon Production by Inducing a Host Shutoff That Requires Accessory Protein 5b.</ArticleTitle>
<Pagination><MedlinePgn>7519-7528</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00627-16</ELocationID>
<Abstract><AbstractText Label="UNLABELLED">During infection of their host cells, viruses often inhibit the production of host proteins, a process that is referred to as host shutoff. By doing this, viruses limit the production of antiviral proteins and increase production capacity for viral proteins. Coronaviruses from the genera Alphacoronavirus and Betacoronavirus, such as severe acute respiratory syndrome coronavirus (SARS-CoV), establish host shutoff via their nonstructural protein 1 (nsp1). The Gammacoronavirus and Deltacoronavirus genomes, however, do not encode nsp1, and it has been suggested that these viruses do not induce host shutoff. Here, we show that the Gammacoronavirus infectious bronchitis virus (IBV) does induce host shutoff, and we find that its accessory protein 5b is indispensable for this function. Importantly, we found that 5b-null viruses, unlike wild-type viruses, induce production of high concentrations of type I interferon protein in vitro, indicating that host shutoff by IBV plays an important role in antagonizing the host's innate immune response. Altogether, we demonstrate that 5b is a functional equivalent of nsp1, thereby answering the longstanding question of whether lack of nsp1 in gammacoronaviruses is compensated for by another viral protein. As such, our study is a significant step forward in the understanding of coronavirus biology and closes a gap in the understanding of some IBV virulence strategies.</AbstractText>
<AbstractText Label="IMPORTANCE">Many viruses inhibit protein synthesis by their host cell to enhance virus replication and to antagonize antiviral defense mechanisms. This process is referred to as host shutoff. We studied gene expression and protein synthesis in chicken cells infected with the important poultry pathogen infectious bronchitis virus (IBV). We show that IBV inhibits synthesis of host proteins, including that of type I interferon, a key component of the antiviral response. The IBV-induced host shutoff, however, does not require degradation of host RNA. Furthermore, we demonstrate that accessory protein 5b of IBV plays a crucial role in the onset of host shutoff. Our findings suggest that inhibition of host protein synthesis is a common feature of coronaviruses and primarily serves to inhibit the antiviral response of the host.</AbstractText>
<CopyrightInformation>Copyright © 2016, American Society for Microbiology. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kint</LastName>
<ForeName>Joeri</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, Wageningen, The Netherlands.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>MSD Animal Health, Bioprocess Technology and Support, Boxmeer, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Langereis</LastName>
<ForeName>Martijn A</ForeName>
<Initials>MA</Initials>
<AffiliationInfo><Affiliation>Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Maier</LastName>
<ForeName>Helena J</ForeName>
<Initials>HJ</Initials>
<AffiliationInfo><Affiliation>Avian Viral Diseases, The Pirbright Institute, Compton Laboratory, Pirbright, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Britton</LastName>
<ForeName>Paul</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Avian Viral Diseases, The Pirbright Institute, Compton Laboratory, Pirbright, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>van Kuppeveld</LastName>
<ForeName>Frank J</ForeName>
<Initials>FJ</Initials>
<AffiliationInfo><Affiliation>Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Koumans</LastName>
<ForeName>Joseph</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>MSD Animal Health, Bioprocess Technology and Support, Boxmeer, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wiegertjes</LastName>
<ForeName>Geert F</ForeName>
<Initials>GF</Initials>
<AffiliationInfo><Affiliation>Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, Wageningen, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Forlenza</LastName>
<ForeName>Maria</ForeName>
<Initials>M</Initials>
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Infectious Bronchitis Coronavirus Limits Interferon Production by Inducing a Host Shutoff That Requires Accessory Protein 5b.

Infectious Bronchitis Coronavirus Limits Interferon Production by Inducing a Host Shutoff That Requires Accessory Protein 5b.

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