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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


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    Targeting pentose phosphate pathway for SARS-CoV-2 therapy

    Authors: Denisa Bojkova; Rui Costa; Marco Bechtel; Sandra Ciesek; Martin Michaelis; Jindrich Cinatl Jr.; Leo C James; Madeline A Lancaster; Zhu Shu; Zhiming Yuan; Lei Tong; Han Xia; Jingzhe Pan; Natalie Garton; Manish Pareek; Michael Barer; Craig J Smith; Stuart M Allan; Michelle M. Lister; Hannah C. Howson-Wells; Edward C Holmes; Matthew W. Loose; Jonathan K. Ball; C. Patrick McClure; - The COVID-19 Genomics UK consortium study group; Shi Chen

    doi:10.1101/2020.08.19.257022 Date: 2020-08-21 Source: bioRxiv

    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.

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MeSH Disease
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SARS-CoV-2 Proteins


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