Author

Y. Hirayama

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Microbiology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2

Frequent Co-Authors

J. Gohda· 2 shared J.-i. Inoue· 2 shared K. Tomita· 2 shared M. Yamamoto· 2 shared Y. Kawaguchi· 2 shared A. Kobayashi· 1 shared K. Semba· 1 shared M. Seiki· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersMicrobiology

J. Gohda

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2 papers

Recent·Most cited

SARS-CoV-2 Omicron spike H655Y mutation is responsible for enhancement of the endosomal entry pathway and reduction of cell surface entry pathway

M. Yamamoto, K. Tomita, Y. Hirayama, J.-i. Inoue, Y. Kawaguchi, J. Gohda

This paper investigates how the H655Y mutation in the Omicron SARS-CoV-2 spike protein enhances endosomal entry and reduces cell surface entry, altering viral tropism and fusogenicity.

bioRxiv · Mar 21, 2022 · PreprintMicrobiology

Metalloproteinase-dependent and TMPRSS2-independnt cell surface entry pathway of SARS-CoV-2 requires the furin-cleavage site and the S2 domain of spike protein

M. Yamamoto, J. Gohda, A. Kobayashi, K. Tomita, Y. Hirayama, N. Koshikawa, M. Seiki, K. Semba, T. Akiyama, Y. Kawaguchi, J.-i. Inoue

This study identifies a TMPRSS2-independent metalloproteinase-dependent entry pathway for SARS-CoV-2 that requires the furin cleavage site and S2 domain of the spike protein, highlighting new therapeutic targets.

bioRxiv · Dec 14, 2021 · PreprintMicrobiology