It becomes more and more obvious that deregulation of host metabolism play an important role in SARS-CoV-2 pathogenesis with implication for increased risk of severe course of COVID-19 MESHD
. Furthermore, it is expected that COVID-19 MESHD
patients recovered from severe disease may experience long-term metabolic disorders MESHD
. Thereby understanding the consequences of SARS-CoV-2 infection MESHD
on host metabolism can facilitate efforts for effective treatment option. We have previously shown that SARS-CoV-2-infected MESHD
cells undergo a shift towards glycolysis and that 2-deoxy-D-glucose (2DG) inhibits SARS-CoV-2 replication. Here, we show that also pentose phosphate pathway (PPP) is remarkably deregulated. Since PPP supplies ribonucleotides for SARS-CoV-2 replication, this could represent an attractive target for an intervention. On that account, we employed the transketolase HGNC
inhibitor benfooxythiamine and showed dose-dependent inhibition of SARS-CoV-2 in non-toxic concentrations. Importantly, the antiviral efficacy of benfooxythiamine was further increased in combination with 2DG.