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SARS-CoV-2 infection rewires host cell metabolism and is potentially susceptible to mTORC1 inhibition.

  • Author(s): Mullen, Peter J
  • Garcia, Gustavo
  • Purkayastha, Arunima
  • Matulionis, Nedas
  • Schmid, Ernst W
  • Momcilovic, Milica
  • Sen, Chandani
  • Langerman, Justin
  • Ramaiah, Arunachalam
  • Shackelford, David B
  • Damoiseaux, Robert
  • French, Samuel W
  • Plath, Kathrin
  • Gomperts, Brigitte N
  • Arumugaswami, Vaithilingaraja
  • Christofk, Heather R
  • et al.

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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