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Using a combination of metabolomics and bacterial and host genetics, Pruss et al. show that upregulated oxidative ornithine metabolism in Clostridioidesdifficile promotes its persistence within the gastrointestinal tract under non-inflammatory conditions.
Zhong et al. show that the protein GP73 stimulates hepatic glucose production and is induced in response to infection with SARS-CoV-2 in vitro and in vivo, thus proposing a molecular mechanism underlying hyperglycemia associated with COVID-19.
Coronavirus replication results in expenditure of nicotinamide adenine dinucleotide (NAD+), the central catalyst of cellular metabolism, in the innate response to infection. Repletion of NAD+ levels has the potential to enhance antiviral responses.