Susan Reich Weiss

This study shows that SARS-CoV-2 defective viral genomes from different genomic hotspots induce divergent interferon responses, with hotspot B DVGs strongly stimulating IFN responses and hotspot A DVGs not.

This study shows adenovirus mutants differentially activate dsRNA sensors, leading to distinct RNP granule assemblies via PKR and OAS3/RNase L pathways.

This study shows that inhibiting RNA splicing reduces viral replication in splicing-dependent viruses like adenovirus, HSV-1, and influenza A, suggesting a new antiviral strategy.

This study uses flow virometry to analyze spike antigenicity of endemic human coronaviruses, revealing cell line-dependent differences and heterogeneity not captured by bulk assays.

This study compares how SARS-CoV-2 and MERS-CoV nsp1 proteins affect host protein synthesis and the integrated stress response, revealing differential impacts on eIF2 phosphorylation and stress granule formation.

This study compares protease utilization in Clade C MERS-CoV camel strains, finding reduced TMPRSS2-mediated entry in East African isolates compared to Clade A/B strains.

This study shows MERS-CoV inhibits PKR activation by blocking its condensation on viral dsRNA, revealing a mechanism by which the virus evades innate immune responses.

This study compares how three betacoronaviruses interact with the PERK pathway of the integrated stress response, showing differences in their reliance on eIF2 dephosphorylation for replication.

The paper examines how interferon signaling in nasal epithelial cells differentiates between common cold and lethal respiratory viruses, showing its role in viral clearance.

This study shows that PKR activation can both restrict and enhance LCMV replication, revealing a complex role for PKR in mammarenavirus infection.