CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry
Elena-Sofia Heinl,
Sebastian Lorenz,
Barbara Schmidt,
Nouf Nasser M Laqtom,
Joseph R. Mazzulli,
Laetitia Francelle,
Timothy W. Yu,
Benjamin Greenberg,
Stephan Storch,
Ines Tegtmeier,
Helga Othmen,
Katja Maurer,
Malin Steinfurth,
Ralph Witzgall,
Vladimir Milenkovic,
Christian H. Wetzel,
Markus Reichold
Affiliations
Elena-Sofia Heinl
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany
Sebastian Lorenz
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany
Barbara Schmidt
Institute of Clinical Microbiology and Hygiene, University of Regensburg, 93053 Regensburg, Germany
Nouf Nasser M Laqtom
Departments of Chemical Engineering and Genetics, Stanford University, Stanford, CA 94305, USA
Joseph R. Mazzulli
The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
Laetitia Francelle
The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
Timothy W. Yu
Division of Genetics and Genomics, Boston Children’s Hospital, Boston, MA, USA; Department of Pediatrics, Harvard Medical School, Boston, MA, USA
Benjamin Greenberg
Department of Neurology, UT Southwestern Medical Center, Dallas, TX, USA
Stephan Storch
Children’s Hospital Biochemistry, University Medical Center Hamburg Eppendorf, 20246 Hamburg, Germany
Ines Tegtmeier
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany
Helga Othmen
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany; Institute for Molecular and Cellular Anatomy, University Regensburg, 93053 Regensburg, Germany
Katja Maurer
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany
Malin Steinfurth
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany
Ralph Witzgall
Institute for Molecular and Cellular Anatomy, University Regensburg, 93053 Regensburg, Germany
Vladimir Milenkovic
Department of Psychiatry and Psychotherapy, University of Regensburg, 93053 Regensburg, Germany
Christian H. Wetzel
Department of Psychiatry and Psychotherapy, University of Regensburg, 93053 Regensburg, Germany
Markus Reichold
Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany; Corresponding author
Summary: The SARS-CoV-2 virus has triggered a worldwide pandemic. According to the BioGrid database, CLN7 (MFSD8) is thought to interact with several viral proteins. The aim of this work was to investigate a possible involvement of CLN7 in the infection process. Experiments on a CLN7-deficient HEK293T cell line exhibited a 90% reduced viral load compared to wild-type cells. This observation may be linked to the finding that CLN7 ko cells have a significantly reduced GM1 content in their cell membrane. GM1 is found highly enriched in lipid rafts, which are thought to play an important role in SARS-CoV-2 infection. In contrast, overexpression of CLN7 led to an increase in viral load. This study provides evidence that CLN7 is involved in SARS-CoV-2 infection. This makes it a potential pharmacological target for drug development against COVID-19. Furthermore, it provides insights into the physiological function of CLN7 where still only little is known about.
