CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry

  • Elena-Sofia Heinl (Geteilte/r Erstautor/in)
  • Sebastian Lorenz (Geteilte/r Erstautor/in)
  • 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

Abstract

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.

Bibliografische Daten

OriginalspracheEnglisch
Aufsatznummer105082
ISSN2589-0042
DOIs
StatusVeröffentlicht - 21.10.2022

Anmerkungen des Dekanats

© 2022.

PubMed 36093380