AI Article Synopsis
- - SARS-CoV-2 infection alters the metabolism of host cells by increasing glucose entry into the TCA cycle and changing how cells process glutamine, which could lead to virus replication.
- - The study confirms that the activation of mTORC1, a key metabolic regulator, occurs in both infected cell cultures and lung tissue from COVID-19 patients.
- - Targeting mTORC1 with inhibitors shows promise in reducing viral replication, indicating a potential treatment strategy for COVID-19 that warrants further investigation.
Article Abstract
Viruses hijack host cell metabolism to acquire the building blocks required for replication. Understanding how SARS-CoV-2 alters host cell metabolism may lead to potential treatments for COVID-19. Here we profile metabolic changes conferred by SARS-CoV-2 infection in kidney epithelial cells and lung air-liquid interface (ALI) cultures, and show that SARS-CoV-2 infection increases glucose carbon entry into the TCA cycle via increased pyruvate carboxylase expression. SARS-CoV-2 also reduces oxidative glutamine metabolism while maintaining reductive carboxylation. Consistent with these changes, SARS-CoV-2 infection increases the activity of mTORC1 in cell lines and lung ALI cultures. Lastly, we show evidence of mTORC1 activation in COVID-19 patient lung tissue, and that mTORC1 inhibitors reduce viral replication in kidney epithelial cells and lung ALI cultures. Our results suggest that targeting mTORC1 may be a feasible treatment strategy for COVID-19 patients, although further studies are required to determine the mechanism of inhibition and potential efficacy in patients.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7994801 | PMC |
| http://dx.doi.org/10.1038/s41467-021-22166-4 | DOI Listing |
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