Bryan A. Johnson

This study shows that disrupting both NSP3 and nucleocapsid SG antagonism reduces SARS-CoV-2 replication and disease, suggesting stress granule activation as a therapeutic target.

This study shows SARS-CoV-2 NSP15 (EndoU) regulates RNA recombination and viral fitness, with its loss reducing replication but increasing inflammation and defective genomes.

This study shows that the furin cleavage site (FCS) is essential for SARS-CoV-2 pathogenesis but not for transmission, as a mutant lacking FCS was transmissible in hamsters but caused less severe disease.

The paper identifies a mutation in the SARS-CoV-2 nucleocapsid protein that enhances viral infection by promoting dimer formation and altering virion structure.

This study identifies a novel interaction between SARS-CoV-2 NSP3 and FMRPs, showing that this interaction is critical for viral replication and disease progression.

This study identifies the role of G3BP1-N interaction in SARS-CoV-2 replication by showing that disrupting this interaction reduces viral replication and pathogenesis.