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Elevation in sphingolipid upon SARS-CoV-2 infection: possible implications for COVID-19 pathology
Einat B Vitner1, Roy Avraham2, Boaz Politi2
1Departments of Infectious Diseases, Israel Institute for Biological Research, Ness-Ziona, Israel einatv@iibr.gov.il.
Life Science Alliance
|November 12, 2021
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection increases sphingolipid (SL) levels, which are crucial for viral replication. Inhibiting glucosylceramide synthase can reverse these elevations, offering potential therapeutic strategies for COVID-19.
Area of Science:
- Biochemistry
- Virology
- Immunology
Background:
- Understanding COVID-19 pathogenesis is crucial for effective disease management and therapeutic development.
- Sphingolipids (SLs) play vital roles in cellular processes, and their dysregulation may impact viral infections.
Purpose of the Study:
- To investigate the alterations in sphingolipid levels during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
- To explore the role of sphingolipids in viral replication and potential therapeutic interventions for COVID-19.
Main Methods:
- Analysis of sphingolipid profiles in cells and serum from SARS-CoV-2 infected mice.
- Assessment of the impact of sphingolipid alterations on viral replication.
- Evaluation of glucosylceramide synthase inhibitors as a therapeutic approach.
Main Results:
- SARS-CoV-2 infection led to a significant elevation of sphingolipid levels in both cellular and serum samples.
- Increased glycosphingolipid levels were observed early in infection and were essential for SARS-CoV-2 replication.
- Specific sphingolipids including sphinganine, sphingosine, GA1, and GM3 were markedly increased.
- Treatment with glucosylceramide synthase inhibitors reversed the elevated sphingolipid levels.
Conclusions:
- Sphingolipid metabolism is altered during SARS-CoV-2 infection.
- Elevated glycosphingolipids are critical for SARS-CoV-2 replication.
- Targeting glucosylceramide synthase presents a potential therapeutic strategy for managing COVID-19.
