K. Tokunaga

This study examines virological parameters of SARS-CoV-2 variants correlating with spike protein fusogenicity, finding strong links with S1/S2 cleavage efficiency and plaque size.

The paper identifies specific residues in the spike protein and ACE2 receptor that determine the host tropism of two SARS-CoV-2-related bat coronaviruses.

This study identifies the cellular origin of aberrant SALL4 expression in MDS using mass cytometry, showing it is mainly in HSPC and myeloid lineages, with SALL4/p53 co-expression linked to TP53 mutations.

The paper investigates the SARS-CoV-2 Lambda variant, finding it more infectious due to specific mutations and better immune evasion, contributing to its spread in South America.

This study shows the P681R mutation in the SARS-CoV-2 spike protein enhances fusogenicity and pathogenicity in the Delta variant compared to the prototypic virus.

This study identifies MARCH8 as an antiviral factor that ubiquitinates and degrades viral envelope glycoproteins by targeting their cytoplasmic lysine residues.

The paper examines how naturally occurring mutations in SARS-CoV-2 spike proteins affect cell entry via ACE2 and TMPRSS2, finding that the D614G mutation increases infectivity but remains neutralization-sensitive.

This paper introduces a HiBiT-based luciferase assay for rapid and accurate quantification of HIV-1 production, outperforming traditional methods like ELISA.

This study identifies two distinct mechanisms by which MARCH8 inhibits viral infection: ubiquitination of VSV-G and tyrosine motif-dependent sorting of HIV-1 Env.