Whereas SARS-CoV-2 utilizes cathepsins to enter most cell lines, human airway organoids revealed that entry into relevant cells is dependent on serine proteases, which can be targeted for treatment.
A novel, overlapping, putatively functional gene in SARS-CoV-2, ORF3d, is absent from close relatives of SARS-CoV-2 and may have contributed to the biology, emergence, or spread of the virus.
3% of >1,000 asymptomatic healthcare workers in their workplace tested positive for SARS-CoV-2, suggesting that comprehensive screening programmes are vital to prevent acquisition of COVID-19 in hospitals.
SARS-CoV-2 spike variants that resist neutralization by therapeutic antibodies or convalescent plasma can be generated in the laboratory and exist at low frequency in natural populations.
Current evidence does not suggest adverse effects of ACE inhibitors or ARBs in COVID-19 patients and, to the contrary, discontinuing these drugs in these patients may potentially be harmful.
Characterisation of SARS-CoV-2 genomic divergence in healthcare-associated outbreaks demonstrates that the inclusion of healthcare workers in contact networks identifies additional links in SARS-CoV-2 transmission pathways.
Transcription changes in cells taken from bronchoalveolar fluid of COVID-19 patients indicate severe disruption of coagulation and fibrinolytic pathways in the lung and suggest similar processes in other organs.
A mutual information algorithm points to macrophage activation syndrome as a specific pathogenic mechanism in COVID-19, correlated with disease severity, which could be used to monitor disease and therapeutics.
