IFITM proteins promote SARS-CoV-2 infection and are targets for virus inhibition in vitro

Caterina Prelli Bozzo, Rayhane Nchioua, Meta Volcic, Lennart Koepke, Jana Krüger, Desiree Schütz, Sandra Heller, Christina M. Stürzel, Dorota Kmiec, Carina Conzelmann, Janis Müller, Fabian Zech, Elisabeth Braun, Rüdiger Groß, Lukas Wettstein, Tatjana Weil, Johanna Weiß, Federica Diofano, Armando A. Rodríguez Alfonso, Sebastian Wiese, Daniel Sauter, Jan Münch, Christine Goffinet, Alberto Catanese, Michael Schön, Tobias M. Boeckers, Steffen Stenger, Kei Sato, Steffen Just, Alexander Kleger, Konstantin M. J. Sparrer () and Frank Kirchhoff ()
Additional contact information
Caterina Prelli Bozzo: Ulm University Medical Center
Rayhane Nchioua: Ulm University Medical Center
Meta Volcic: Ulm University Medical Center
Lennart Koepke: Ulm University Medical Center
Jana Krüger: Ulm University Medical Center
Desiree Schütz: Ulm University Medical Center
Sandra Heller: Ulm University Medical Center
Christina M. Stürzel: Ulm University Medical Center
Dorota Kmiec: Ulm University Medical Center
Carina Conzelmann: Ulm University Medical Center
Janis Müller: Ulm University Medical Center
Fabian Zech: Ulm University Medical Center
Elisabeth Braun: Ulm University Medical Center
Rüdiger Groß: Ulm University Medical Center
Lukas Wettstein: Ulm University Medical Center
Tatjana Weil: Ulm University Medical Center
Johanna Weiß: Ulm University Medical Center
Federica Diofano: Ulm University
Armando A. Rodríguez Alfonso: Ulm University Medical Center
Sebastian Wiese: Ulm University Medical Center
Daniel Sauter: Ulm University Medical Center
Jan Münch: Ulm University Medical Center
Christine Goffinet: Charité—Universitätsmedizin Berlin
Alberto Catanese: Ulm University
Michael Schön: Ulm University
Tobias M. Boeckers: Ulm University
Steffen Stenger: Ulm University Medical Center
Kei Sato: The University of Tokyo
Steffen Just: Ulm University
Alexander Kleger: Ulm University Medical Center
Konstantin M. J. Sparrer: Ulm University Medical Center
Frank Kirchhoff: Ulm University Medical Center

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) can restrict viral pathogens, but pro- and anti-viral activities have been reported for coronaviruses. Here, we show that artificial overexpression of IFITMs blocks SARS-CoV-2 infection. However, endogenous IFITM expression supports efficient infection of SARS-CoV-2 in human lung cells. Our results indicate that the SARS-CoV-2 Spike protein interacts with IFITMs and hijacks them for efficient viral infection. IFITM proteins were expressed and further induced by interferons in human lung, gut, heart and brain cells. IFITM-derived peptides and targeting antibodies inhibit SARS-CoV-2 entry and replication in human lung cells, cardiomyocytes and gut organoids. Our results show that IFITM proteins are cofactors for efficient SARS-CoV-2 infection of human cell types representing in vivo targets for viral transmission, dissemination and pathogenesis and are potential targets for therapeutic approaches.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24817-y

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DOI: 10.1038/s41467-021-24817-y

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