A. Takaori-Kondo

This study investigates the virological characteristics of SARS-CoV-2 Omicron BA.2.75, finding it has higher transmissibility and pathogenicity compared to BA.2 and BA.5, but similar sensitivity to antiviral drugs.

This study identifies the S375F mutation in the Omicron spike protein as responsible for its reduced cleavage efficiency, fusogenicity, and rapid spread.

This study compares the virological characteristics of SARS-CoV-2 BA.2 and BA.1 variants, finding BA.2 has higher transmissibility, different antigenicity, greater replicative capacity, and higher pathogenicity in hamsters.

This study identifies mutations in the SARS-CoV-2 Mu variant responsible for its immune resistance and shows that Mu-infected convalescent sera are broadly antiviral.

This study shows that Mu variant is highly resistant to neutralization by convalescent and vaccine sera compared to other variants.

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 the HBO1-MLL interaction as critical for leukemogenesis by facilitating the AF4/ENL/P-TEFb complex-mediated gene activation in MLL fusion proteins.

This study identifies ORF66's critical role in KSHV late gene expression and viral production by interacting with ORF34 and binding to the K8.1 promoter.

The paper develops APOBEC3B reporter myeloma cell lines to study DNA damage response pathways that regulate APOBEC3B expression, finding that conventional therapies increase its expression while targeted drugs do not.