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

doi:10.1016/j.isci.2022.105082

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^*

^*Corresponding author for this work

Bioscience

Research output: Contribution to journal › Article › peer-review

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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.

Original language	English (US)
Article number	105082
Journal	iScience
Volume	25
Issue number	10
DOIs	https://doi.org/10.1016/j.isci.2022.105082
State	Published - Oct 21 2022

Keywords

Cell biology
Virology

ASJC Scopus subject areas

General

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10.1016/j.isci.2022.105082

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Heinl, E. S., Lorenz, S., Schmidt, B., Nasser M Laqtom, N., Mazzulli, J. R., Francelle, L., Yu, T. W., Greenberg, B., Storch, S., Tegtmeier, I., Othmen, H., Maurer, K., Steinfurth, M., Witzgall, R., Milenkovic, V., Wetzel, C. H., & Reichold, M. (2022). CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry. iScience, 25(10), Article 105082. https://doi.org/10.1016/j.isci.2022.105082

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title = "CLN7/MFSD8 may be an important factor for SARS-CoV-2 cell entry",

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.",

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author = "Heinl, {Elena Sofia} and Sebastian Lorenz and Barbara Schmidt and {Nasser M Laqtom}, Nouf and Mazzulli, {Joseph R.} and Laetitia Francelle and Yu, {Timothy W.} and Benjamin Greenberg and Stephan Storch and Ines Tegtmeier and Helga Othmen and Katja Maurer and Malin Steinfurth and Ralph Witzgall and Vladimir Milenkovic and Wetzel, {Christian H.} and Markus Reichold",

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year = "2022",

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doi = "10.1016/j.isci.2022.105082",

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AU - Heinl, Elena Sofia

AU - Lorenz, Sebastian

AU - Schmidt, Barbara

AU - Nasser M Laqtom, Nouf

AU - Mazzulli, Joseph R.

AU - Francelle, Laetitia

AU - Yu, Timothy W.

AU - Greenberg, Benjamin

AU - Storch, Stephan

AU - Tegtmeier, Ines

AU - Othmen, Helga

AU - Maurer, Katja

AU - Steinfurth, Malin

AU - Witzgall, Ralph

AU - Milenkovic, Vladimir

AU - Wetzel, Christian H.

AU - Reichold, Markus

PY - 2022/10/21

Y1 - 2022/10/21

N2 - 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.

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

Abstract

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