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

View ORCID ProfileThomas P. Peacock, View ORCID ProfileCarol M. Sheppard, View ORCID ProfileJonathan C. Brown, View ORCID ProfileNiluka Goonawardane, View ORCID ProfileJie Zhou, View ORCID ProfileMax Whiteley, PHE Virology Consortium, View ORCID ProfileThushan I. de Silva, View ORCID ProfileWendy S. Barclay
doi: https://doi.org/10.1101/2021.05.28.446163
Thomas P. Peacock
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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Carol M. Sheppard
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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Jonathan C. Brown
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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Niluka Goonawardane
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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Jie Zhou
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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Max Whiteley
2The Florey Institute for Host-Pathogen Interactions and Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, UK, S10 2RX
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3Public Health England, UK
Thushan I. de Silva
2The Florey Institute for Host-Pathogen Interactions and Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, UK, S10 2RX
4South Yorkshire Regional Department of Infection and Tropical Medicine, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK, S10 2JF
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Wendy S. Barclay
1Department of Infectious Disease, Imperial College London, UK, W2 1PG
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  • For correspondence: w.barclay@imperial.ac.uk
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Abstract

The spike (S) glycoprotein of the SARS-CoV-2 virus that emerged in 2019 contained a suboptimal furin cleavage site at the S1/S2 junction with the sequence 681PRRAR/S686. This cleavage site is required for efficient airway replication, transmission, and pathogenicity of the virus. The B.1.617 lineage has recently emerged in India, coinciding with substantial disease burden across the country. Early evidence suggests that B.1.617.2 (a sublineage of B.1.617) is more highly transmissible than contemporary lineages. B.1.617 and its sublineages contain a constellation of S mutations including the substitution P681R predicted to further optimise this furin cleavage site. We provide experimental evidence that virus of the B.1.617 lineage has enhanced S cleavage, that enhanced processing of an expressed B.1.617 S protein in cells is due to P681R, and that this mutation enables more efficient cleavage of a peptide mimetic of the B.1.617 S1/S2 cleavage site by recombinant furin. Together, these data demonstrate viruses in this emerging lineage have enhanced S cleavage by furin which we hypothesise could be enhancing transmissibility and pathogenicity.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted May 28, 2021.
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The SARS-CoV-2 variants associated with infections in India, B.1.617, show enhanced spike cleavage by furin
Thomas P. Peacock, Carol M. Sheppard, Jonathan C. Brown, Niluka Goonawardane, Jie Zhou, Max Whiteley, PHE Virology Consortium, Thushan I. de Silva, Wendy S. Barclay
bioRxiv 2021.05.28.446163; doi: https://doi.org/10.1101/2021.05.28.446163
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The SARS-CoV-2 variants associated with infections in India, B.1.617, show enhanced spike cleavage by furin
Thomas P. Peacock, Carol M. Sheppard, Jonathan C. Brown, Niluka Goonawardane, Jie Zhou, Max Whiteley, PHE Virology Consortium, Thushan I. de Silva, Wendy S. Barclay
bioRxiv 2021.05.28.446163; doi: https://doi.org/10.1101/2021.05.28.446163

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