When antiviral compounds target oligomeric assemblages, the formation of chimeric oligomers within cells can negate selection for naturally occurring drug-resistant variants.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

New mammarenaviruses have been identified from rodents in Cambodia and Thailand, and the Cardamones variant of Wēnzhōu virus has been found in Cambodian patients presenting with fever and respiratory symptoms.

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

RNA virus replication is attenuated by an intrinsic restriction mechanism after introducing CpG/UpA dinucleotides into both non-translated and coding regions of viral genomes, which may be exploited in the design of attenuated virus vaccines.

A picorna-like virus promotes the accumulation of caspase-cleaved drosophila inhibitor of apoptosis 1 by inducing the degradation of NTAN1, a key N-end rule degradation pathway component, leading to apoptosis inhibition and viral replication enhancement.

Rotavirus infection induces phosphorylation and proteasomal degradation of MAVS to suppress host antiviral interferon signaling.

Quasi-enveloped hepatitis A virions undergo clathrin-mediated endocytosis, followed by ALIX-dependent trafficking to lysosomes where the quasi-envelope is degraded, triggering uncoating of the RNA genome in association with lysosomal membrane rupture.

Using a suite of CRISPR technologies, unique chemical tools, and carefully designed biochemical and cell biological assays, we define the mechanism of action of Retro-2, an inhibitor of retrograde toxins.

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