IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms
Identifieur interne : 001636 ( Main/Exploration ); précédent : 001635; suivant : 001637IFITM Proteins Inhibit Entry Driven by the MERS-Coronavirus Spike Protein: Evidence for Cholesterol-Independent Mechanisms
Auteurs : Florian Wrensch ; Michael Winkler ; Stefan PöhlmannSource :
- Viruses [ 1999-4915 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Antigènes de différenciation (génétique), Antigènes de différenciation (métabolisme), Cellules HEK293, Cholestérol (métabolisme), Coronavirus du syndrome respiratoire du Moyen-Orient (physiologie), Expression des gènes, Glycoprotéine de spicule des coronavirus (métabolisme), Humains, Infections à coronavirus (génétique), Infections à coronavirus (métabolisme), Lignée cellulaire, Protéines de liaison à l'ARN (génétique), Protéines de liaison à l'ARN (métabolisme), Protéines membranaires (génétique), Protéines membranaires (métabolisme), Pénétration virale, Transport biologique.
- MESH :
- génétique : Antigènes de différenciation, Infections à coronavirus, Protéines de liaison à l'ARN, Protéines membranaires.
- métabolisme : Antigènes de différenciation, Cholestérol, Glycoprotéine de spicule des coronavirus, Infections à coronavirus, Protéines de liaison à l'ARN, Protéines membranaires.
- physiologie : Coronavirus du syndrome respiratoire du Moyen-Orient.
- Animaux, Cellules HEK293, Expression des gènes, Humains, Lignée cellulaire, Pénétration virale, Transport biologique.
English descriptors
- KwdEn :
- Animals, Antigens, Differentiation (genetics), Antigens, Differentiation (metabolism), Biological Transport, Cell Line, Cholesterol (metabolism), Coronavirus Infections (genetics), Coronavirus Infections (metabolism), Gene Expression, HEK293 Cells, Humans, Membrane Proteins (genetics), Membrane Proteins (metabolism), Middle East Respiratory Syndrome Coronavirus (physiology), RNA-Binding Proteins (genetics), RNA-Binding Proteins (metabolism), Spike Glycoprotein, Coronavirus (metabolism), Virus Internalization.
- MESH :
- chemical , genetics : Antigens, Differentiation, Membrane Proteins, RNA-Binding Proteins.
- chemical , metabolism : Antigens, Differentiation, Cholesterol, Membrane Proteins, RNA-Binding Proteins, Spike Glycoprotein, Coronavirus.
- genetics : Coronavirus Infections.
- metabolism : Coronavirus Infections.
- physiology : Middle East Respiratory Syndrome Coronavirus.
- Animals, Biological Transport, Cell Line, Gene Expression, HEK293 Cells, Humans, Virus Internalization.
Abstract
The interferon-inducible transmembrane (IFITM) proteins 1, 2 and 3 inhibit the host cell entry of several enveloped viruses, potentially by promoting the accumulation of cholesterol in endosomal compartments. IFITM3 is essential for control of influenza virus infection in mice and humans. In contrast, the role of IFITM proteins in coronavirus infection is less well defined. Employing a retroviral vector system for analysis of coronavirus entry, we investigated the susceptibility of human-adapted and emerging coronaviruses to inhibition by IFITM proteins. We found that entry of the recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV) is sensitive to inhibition by IFITM proteins. In 293T cells, IFITM-mediated inhibition of cellular entry of the emerging MERS- and SARS-CoV was less efficient than blockade of entry of the globally circulating human coronaviruses 229E and NL63. Similar differences were not observed in A549 cells, suggesting that cellular context and/or IFITM expression levels can impact inhibition efficiency. The differential IFITM-sensitivity of coronaviruses observed in 293T cells afforded the opportunity to investigate whether efficiency of entry inhibition by IFITMs and endosomal cholesterol accumulation correlate. No such correlation was observed. Furthermore, entry mediated by the influenza virus hemagglutinin was robustly inhibited by IFITM3 but was insensitive to accumulation of endosomal cholesterol, indicating that modulation of cholesterol synthesis/transport did not account for the antiviral activity of IFITM3. Collectively, these results show that the emerging MERS-CoV is a target of the antiviral activity of IFITM proteins and demonstrate that mechanisms other than accumulation of endosomal cholesterol can contribute to viral entry inhibition by IFITMs.
Url:
DOI: 10.3390/v6093683
PubMed: 25256397
PubMed Central: 4189045
Affiliations:
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Le document en format XML
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respiratoire du Moyen-Orient</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Transport</term><term>Cell Line</term><term>Gene Expression</term><term>HEK293 Cells</term><term>Humans</term><term>Virus Internalization</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HEK293</term><term>Expression des gènes</term><term>Humains</term><term>Lignée cellulaire</term><term>Pénétration virale</term><term>Transport biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The interferon-inducible transmembrane (IFITM) proteins 1, 2 and 3 inhibit the host cell entry of several enveloped viruses, potentially by promoting the accumulation of cholesterol in endosomal compartments. IFITM3 is essential for control of influenza virus infection in mice and humans. In contrast, the role of IFITM proteins in coronavirus infection is less well defined. Employing a retroviral vector system for analysis of coronavirus entry, we investigated the susceptibility of human-adapted and emerging coronaviruses to inhibition by IFITM proteins. We found that entry of the recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV) is sensitive to inhibition by IFITM proteins. In 293T cells, IFITM-mediated inhibition of cellular entry of the emerging MERS- and SARS-CoV was less efficient than blockade of entry of the globally circulating human coronaviruses 229E and NL63. Similar differences were not observed in A549 cells, suggesting that cellular context and/or IFITM expression levels can impact inhibition efficiency. The differential IFITM-sensitivity of coronaviruses observed in 293T cells afforded the opportunity to investigate whether efficiency of entry inhibition by IFITMs and endosomal cholesterol accumulation correlate. No such correlation was observed. Furthermore, entry mediated by the influenza virus hemagglutinin was robustly inhibited by IFITM3 but was insensitive to accumulation of endosomal cholesterol, indicating that modulation of cholesterol synthesis/transport did not account for the antiviral activity of IFITM3. Collectively, these results show that the emerging MERS-CoV is a target of the antiviral activity of IFITM proteins and demonstrate that mechanisms other than accumulation of endosomal cholesterol can contribute to viral entry inhibition by IFITMs.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Holmes, K V" uniqKey="Holmes K">K.V. 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Kupcsik</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Pohlmann, Stefan" sort="Pohlmann, Stefan" uniqKey="Pohlmann S" first="Stefan" last="Pöhlmann">Stefan Pöhlmann</name><name sortKey="Winkler, Michael" sort="Winkler, Michael" uniqKey="Winkler M" first="Michael" last="Winkler">Michael Winkler</name><name sortKey="Wrensch, Florian" sort="Wrensch, Florian" uniqKey="Wrensch F" first="Florian" last="Wrensch">Florian Wrensch</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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