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STING Orchestrates EV-D68 Replication and Immunometabolism within Viral-Induced Replication Organelles
Kathy Triantafilou1, Barbara Szomolay1, Mark William Shepherd1
1Division of Infection and Immunity, School of Medicine, University Hospital of Wales, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Viruses
|October 26, 2024
Summary
The stimulator of interferon genes (STING) pathway, typically for DNA viruses, is hijacked by RNA viruses like SARS-CoV-2 and EV-D68. It aids in forming replication organelles and influences cell metabolism.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Respiratory viruses like Human Rhinovirus, SARS-CoV-2, and Enterovirus D-68 (EV-D68) utilize host lipids to create replication organelles (ROs).
- The stimulator of interferon genes (STING) pathway is a key component of the innate immune system's DNA virus sensing machinery, primarily controlling type I interferon production.
- The role of the STING pathway in RNA viral infections remains largely unexplored despite its established function in DNA virus sensing.
Purpose of the Study:
- To investigate the role of the STING pathway in the replication of RNA viruses that form ROs, specifically EV-D68 and SARS-CoV-2.
- To determine if STING is hijacked by these RNA viruses for their replication machinery and organelle formation.
- To explore the potential link between STING, viral replication, and cellular metabolism.
Main Methods:
- Genetic and pharmacological inhibition of the STING pathway.
- Co-localization studies of STING with viral replication components and host cell proteins.
- Analysis of cellular glucose metabolism in virus-infected cells with and without STING inhibition.
Main Results:
- STING is utilized by EV-D68 and SARS-CoV-2 for replication, indicating a non-canonical function in RNA virus infection.
- STING co-localizes with glycolytic enzymes, suggesting a role in fueling viral replication energetically.
- Inhibition of STING modulates glucose metabolism in EV-D68-infected cells, pointing to potential immunometabolism manipulation.
Conclusions:
- The STING pathway plays a non-canonical role in membrane lipid remodeling and replication vesicle formation for RO-generating RNA viruses.
- STING appears to influence immunometabolism, particularly glucose metabolism, during RNA virus infections.
- These findings reveal a novel function of STING beyond its canonical role in DNA sensing, impacting RNA virus replication and host cell metabolism.
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