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.

The success of angiotensin-converting enzyme 2 (ACE2)-based predictions of severe acute respiratory syndrome-associated virus 2 (SARS-CoV-2) host range stems from phylogenetic correlation, allowing development of scalable models which predict susceptibility to SARS-CoV-2 and other sarbecoviruses without requiring additional ACE2 sequencing.

In the context of SARS-CoV-2 infection, Nsp14 alters gene expression of the host cell through the interaction with the cellular enzyme IMPDH2.

COVID-19 mRNA vaccine-elicited T cells recognize variants of concern and phenotypically differ depending on number of vaccine doses and prior SARS-CoV-2 infection status.

Exploration of the phenotype space corresponding to the sequence space of viable SARS-CoV-2 nucleocapsid protein species reveals significant diversity of biophysical characteristics, nonlocal mutation effects, and functional constraints.

A newly developed lateral flow assay can diagnose mutational signatures of major SARS CoV-2 variants in a rapid, inexpensive, and sequence-free manner.

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.

An in-depth exploratory analysis of the evolutionary and epidemiological dynamics of SARS-CoV-2 in Mexico during the first year of the epidemic provides an overview of different virus dynamics between the developing and developed world (represented by the USA and Mexico).

Lys417 regulates the opening and closing of SARS-CoV-2 spike protein, allowing SARS-CoV-2 to maintain a delicate balance between infectiousness and evading host immune response.

New evidence of brain proinflammatory cascades supports post-acute sequelae of SARS-CoV-2 infection, ultimately promoting the onset and progression of Alzheimer's disease as a function of age.