Enterovirus A71 adaptation to bind heparan sulfate as receptor comes with compensation that destabilizes its virus capsid.

Longitudinal transcriptomic analysis of unvaccinated patients reveals that early NK cell cytotoxicity activation distinguishes mild from severe COVID-19, supporting the relevance of concerted innate–adaptive immune responses against the virus.

Enterovirus D68, a pathogen associated with a rare child paralysis disease, depends on the cellular protein SIRT-1 for release of virus, indicating that SIRT-1 may be an important therapeutic target.

Serocatalytic models applied to seroprevalence data from England reveal an increase in Enterovirus D68 transmission that occurred before 2011.

Evolution-guided functional analyses identify an activating adaptor of the dynein intracellular transportation machinery, NINL, as a novel component of the antiviral immune response and reveal a mechanism by which viruses antagonize NINL function in a species-specific manner.

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.

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.

Proteases from diverse viruses, the first described pathogen-encoded activators of human NLRP1, cleave NLRP1 at a sequence that mimics the viral polyprotein, resulting in inflammasome activation and pro-inflammatory cytokine release.

Genetic and biochemical analyses identify a pathway important for infection by many picornaviruses.

CypA boosts RIG-I-mediated antiviral immune responses via enhancing K63-linked ubiquitination of RIG-I and inhibiting K48-linked ubiquitination of MAVS.