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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Nat+Commun 2021 ; 12 (1): 1876 Nephropedia Template TP
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SARS-CoV-2 infection rewires host cell metabolism and is potentially susceptible to mTORC1 inhibition #MMPMID33767183
Mullen PJ; Garcia G Jr; Purkayastha A; Matulionis N; Schmid EW; Momcilovic M; Sen C; Langerman J; Ramaiah A; Shackelford DB; Damoiseaux R; French SW; Plath K; Gomperts BN; Arumugaswami V; Christofk HR
Nat Commun 2021[Mar]; 12 (1): 1876 PMID33767183show ga
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.
|Animals[MESH]
|Benzamides/pharmacology[MESH]
|COVID-19/*pathology[MESH]
|Cell Line[MESH]
|Chlorocebus aethiops[MESH]
|Citric Acid Cycle/*physiology[MESH]
|Glucose/metabolism[MESH]
|Glutamine/metabolism[MESH]
|HEK293 Cells[MESH]
|Humans[MESH]
|Lung/metabolism/virology[MESH]
|Mechanistic Target of Rapamycin Complex 1/*antagonists & inhibitors/*metabolism[MESH]