iScience (Oct 2022)

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

Journal volume & issue
Vol. 25, no. 10
p. 105082

Abstract

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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.

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