Author

PHE Virology Consortium

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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 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Assay:proteomics· 1 Research Focus:variant effect prediction· 1 Approach:wet-lab / biochemical assay· 1

Frequent Co-Authors

J. C. Brown· 2 shared J. Zhou· 2 shared N. Goonawardane· 2 shared T. P. Peacock· 2 shared W. S. Barclay· 2 shared A. Pinto· 1 shared A. Singanayagam· 1 shared C. M. Sheppard· 1 shared

Activity by Year

2021-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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2 shared papersMicrobiology

J. C. Brown

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2 papers

Recent·Most cited

The SARS-CoV-2 variants associated with infections in India, B.1.617, show enhanced spike cleavage by furin

T. P. Peacock, C. M. Sheppard, J. C. Brown, N. Goonawardane, J. Zhou, M. Whiteley, PHE Virology Consortium, T. I. de Silva, W. S. Barclay

This study shows SARS-CoV-2 B.1.617 variants have enhanced spike cleavage by furin due to the P681R mutation, potentially increasing transmissibility and pathogenicity.

bioRxiv · May 28, 2021 · PreprintMicrobiology

Increased transmission of SARS-CoV-2 lineage B.1.1.7 (VOC 2020212/01) is not accounted for by a replicative advantage in primary airway cells or antibody escape

J. C. Brown, D. H. Goldhill, J. Zhou, T. P. Peacock, R. Frise, N. Goonawardane, L. Baillon, R. Kugathasan, A. Pinto, P. F. McKay, J. Hassard, M. Moshe, A. Singanayagam, T. Burgoyne, the ATACCC Investigators, , W. S. Barclay

This study shows that SARS-CoV-2 variant B.1.1.7 does not replicate better in airway cells or escape antibodies, suggesting its increased transmissibility is due to other factors.

bioRxiv · Feb 24, 2021 · PreprintMicrobiology