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Cholesterol and COVID-19-therapeutic opportunities at the host/virus interface during cell entry

Thomas Grewal1, Mai Khanh Linh Nguyen1, Christa Buechler2

  • 1School of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, Australia.

Life Science Alliance
|February 22, 2024
PubMed

Insights

Targeting cellular cholesterol is a promising strategy against SARS-CoV-2 infection. Drugs affecting cholesterol levels may reduce COVID-19 severity by blocking viral entry and replication.

Area of Science:

  • Virology
  • Cell Biology
  • Pharmacology

Background:

  • The emergence of SARS-CoV-2 variants necessitates novel therapeutic strategies beyond vaccines.
  • Host factors, such as cellular cholesterol, play crucial roles in viral infection cycles.

Purpose of the Study:

  • To review the multifaceted roles of cholesterol in SARS-CoV-2 entry and replication.
  • To explore the therapeutic potential of targeting cholesterol homeostasis for COVID-19 treatment.

Main Methods:

  • Literature review of studies investigating cholesterol's role in SARS-CoV-2 infection.
  • Analysis of pharmacological agents targeting cholesterol pathways for antiviral activity.

Main Results:

  • Cholesterol is essential for SARS-CoV-2 spike protein binding and cell entry.
  • Viral exit from endosomes and new particle release are cholesterol-dependent processes.
  • Statins, PCSK9 inhibitors, ezetimibe, and antifungals show potential in inhibiting SARS-CoV-2.

Conclusions:

  • Cholesterol homeostasis is a critical target for developing new anti-SARS-CoV-2 therapies.
  • Pharmacological interventions modulating cholesterol can reduce viral infectivity and mitigate COVID-19 severity.

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