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

Elena-Sofia Heinl1, Sebastian Lorenz1, Barbara Schmidt2

  • 1Medical Cell Biology, University Regensburg, 93053 Regensburg, Germany.

Iscience
|September 12, 2022
PubMed

Insights

This study reveals CLN7 protein is crucial for SARS-CoV-2 infection. Reducing CLN7 significantly lowers viral load, identifying it as a potential drug target for COVID-19 treatment.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Medicine

Background:

  • Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes a global pandemic.
  • CLN7 (MFSD8) is a protein suggested to interact with SARS-CoV-2 proteins.
  • The role of CLN7 in viral infection remains largely unknown.

Purpose of the Study:

  • To investigate the involvement of CLN7 in the SARS-CoV-2 infection process.
  • To explore CLN7 as a potential therapeutic target for COVID-19.

Main Methods:

  • Utilized CLN7-deficient HEK293T cell lines and wild-type controls.
  • Quantified viral load in cells with altered CLN7 expression.
  • Assessed GM1 ganglioside content in cell membranes.

Main Results:

  • CLN7-deficient cells showed a 90% reduction in SARS-CoV-2 viral load compared to wild-type.
  • CLN7 knockout cells exhibited significantly reduced GM1 ganglioside levels in their cell membrane.
  • Overexpression of CLN7 resulted in an increased viral load.

Conclusions:

  • CLN7 plays a significant role in facilitating SARS-CoV-2 infection.
  • Reduced GM1 ganglioside content in CLN7-deficient cells may impair viral entry.
  • CLN7 represents a promising pharmacological target for developing novel COVID-19 therapeutics.
Keywords:
Cell biologyVirology

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