Characterisation of within-host diversity of SARS-CoV-2 provides insights into the mutational and selective mechanisms driving its evolution and has important implications for using within-host variation to inform transmission inference efforts.
Cell culture adaptation of SARS-CoV-2 is prevented on human airway cells with an active serine protease-mediated entry pathway, allowing the production of genetically stable virus stocks for laboratory experiments.
COVID-19 severity, rather than sex or age, predicts SARS-CoV-2 kinetics, and SARS-CoV-2 viral load from lower respiratory tract specimens may predict severe disease days before clinical deterioration for COVID-19 patients.
High-throughput and ultra-stable magnetic tweezers reveal that Remdesivir induces a long-lived backtrack pause upon incorporation by the coronavirus polymerase, and SARS-CoV-2 is able to evade interferon-induced antiviral ddhCTP.
SARS-CoV-2 has evolved to cleverly mimic the FURIN-cleavage site in human ENaC-α, unlike any prior coronavirus strain, shedding new light on the Acute Respiratory Distress Syndrome (ARDS) in COVID-19 patients.