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Viruses, including SARS-CoV-2, retain infectivity longer at low temperatures and extreme relative humidities because these conditions slow down the chemical reactions that inactivate those viruses.

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.

Molecular dynamics simulation assisted engineering of recombinant soluble human ACE2 N-glycosylation by site-directed mutagenesis or glycosidase treatment yields a superior SARS-CoV-2 decoy receptor.

Cross-reactive T cell immunity against the SARS-CoV-2 is severely compromised in HIV viremic individual.

A model-based approach for modelling the immune control of viral dynamics is applied to quantify the effect of several SARS-CoV-2 vaccine platforms and to define mechanistic correlates of protection.

Immuno-affinity enrichment combined with liquid chromatography-mass spectrometry can be used to detect viral proteins to confirm the presence of SARS-CoV-2 in clinical samples.

Broader case variation in respiratory viral load, and in shedding virus via droplets and aerosols, for SARS-CoV-2 than influenza A(H1N1)pdm09 facilitates greater transmission heterogeneity in the COVID-19 pandemic than the 2009 flu pandemic.

Genomic analysis of initial SARS-CoV-2 waves in Kenya revealed Mombasa City as a key gateway for variants entering Coastal Kenya with onward inter-county transmission highlighting significance of surveillance in major cities for early warning of lineages entering local populations.

An experimental animal model provides further insights into the host and viral mechanisms underlying airborne transmission of SARS-CoV-2.

Only three Spike mutations enable murine SARS-CoV-2 infection, which is still strictly ACE2 dependent and causes a COVID-19-like disease in mice with immunopathology-driven lung damage.