Author

S. T. Yeung

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 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 3 Organism:mouse· 3 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

K. M. Khanna· 3 shared B. A. Rodriguez-Rodriguez· 2 shared C. Loomis· 2 shared A. Hine· 1 shared A. M. Valero-Jimenez· 1 shared A. Schinlever· 1 shared D. Hudesman· 1 shared D. Li· 1 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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3 shared papersMicrobiology

K. M. Khanna

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A neonatal mouse model characterizes transmissibility of SARS-CoV-2 variants and reveals a role for ORF8

B. A. Rodriguez-Rodriguez, G. Ciabattoni, R. Duerr, A. M. Valero-Jimenez, S. T. Yeung, K. M. Crosse, A. Schinlever, L. Bernard-Raichon, J. J. Rodriguez-Galvan, M. McGrath, S. Vashee, Y. Xue, C. Loomis, K. M. Khanna, K. H. Cadwell, , M. Dittmann

This study establishes a neonatal mouse model to study SARS-CoV-2 transmissibility, showing variant differences in infectious shedding and identifying ORF8's role in transmission.

bioRxiv · Oct 4, 2022 · PreprintMicrobiology

MAVS signaling is required for clearance of chikungunya heart infection and prevention of chronic inflammation in vascular tissue

M. G. Noval, S. N. Spector, E. Bartnicki, F. Izzo, N. Narula, S. T. Yeung, P. Damani-Yokota, M. Z. Dewan, V. Mezzano, B. A. Rodriguez-Rodriguez, C. Loomis, K. M. Khanna, K. A. Stapleford

This study investigates CHIKV-induced heart disease using mouse models and human cells, showing MAVS signaling is critical for viral clearance and preventing chronic vascular inflammation.

bioRxiv · May 27, 2022 · PreprintMicrobiology

Serum Amyloid A Proteins Induce Pathogenic TH17 Cells and Promote Inflammatory Disease

J.-Y. Lee, J. A. Hall, L. Kroehling, L. Wu, T. Najar, H. H. Nguyen, W.-Y. Lin, S. T. Yeung, H. M. Silva, D. Li, A. Hine, P. Loke, D. Hudesman, J. C. Martin, E. Kenigsberg, , D. R. Littman

This study shows serum amyloid A proteins drive pathogenic TH17 cell differentiation and promote inflammatory disease through STAT3-activating cytokines.

bioRxiv · Jun 25, 2019Immunology