Kumari G. Lokugamage

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 identifies key residues in SARS-CoV-2 NSP3 that are critical for FXR1 binding and stress granule disruption, showing their role in viral replication and pathogenesis.

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.