RSV's unique ability to co-opt host cell mitochondria to facilitate viral infection reveals the RSV-mitochondrial interface as a viable target for therapeutic intervention.

Patients exposed to ⍺1-AR antagonists have reduced risks of mechanical ventilation and death in lower respiratory tract infection-related illnesses, highlighting the need for prospective trials assessing ⍺1-AR antagonists' effectiveness in COVID-19.

Combined analyses of publicly available population-level variant data and detailed individual-level clinical data can be used to quantify the clinical impact of new SARS-CoV-2 variants in different settings.

Interferon-λ plays a decisive and previously underestimated role in limiting the spread of respiratory viruses from the nasal cavity to the lungs and it efficiently restricts virus transmission from infected individuals to naïve contacts.

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.

Nosocomial transmission of SARS-Cov-2 in geriatric settings is complex, with different patterns between patients and healthcare workers working in Covid/non-Covid wards that should be taken into account when designing infection control strategies.

Population-level hybrid immunity depends substantially on vaccination coverage, including among those previously infected, and dried blood spot collection serves as a practicable biological surveillance platform for these immune responses.

The overall mortality consequences of the COVID-19 pandemic in the United States are predominantly attributable to the direct impact of SARS-CoV-2 infection but there are substantial indirect effects among children and young adults, and in mortality from accidents, homicides, and overdoses.

Proton pump inhibitors are associated with an increased susceptibility to respiratory infections.

Parallel studies in primary human airway cells and stem cell-derived enteroids show that Enterovirus D-68 differentially infects and induces innate immune signaling in the respiratory and intestinal epithelium.