Metabolic Perturbation Associated With COVID-19 Disease Severity and SARS-CoV-2 Replication
Shuba Krishnan, Hampus Nordqvist, Anoop T. Ambikan, Soham Gupta, Maike Sperk, Sara Svensson Akusjärvi, Flora Mikaeloff, Rui Benfeitas, Elisa Saccon, Sivasankaran Munusamy Ponnan, Jimmy Rodriguez Murillo, Negin Nikouyan, Amani Odeh, Gustaf Ahlén, Muhammad Asghar, Matti Sällberg, Jan Vesterbacka, Piotr Nowak, Ákos Végvári, Anders Sönnerborg, Carl Johan Treutiger, Ujjwal Neogi
Abstract
T cells, intermediate and nonclassical monocytes, and amino acid transporter, xCT, in classical, intermediate, and nonclassical monocytes. In in vitro lung epithelial cell (Calu-3) infection model, we found that glycolysis and glutaminolysis are essential for virus replication, and blocking these metabolic pathways caused significant reduction in virus production. Taken together, we therefore hypothesized that severe acute respiratory syndrome coronavirus-2 utilizes and rewires pathways governing central carbon metabolism leading to the efflux of toxic metabolites and associated with disease severity. Thus, the host metabolic perturbation could be an attractive strategy to limit the viral replication and disease severity.