SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway
Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid...
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| Published in | Nature microbiology Vol. 7; no. 8; pp. 1161 - 1179 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.08.2022
Nature Publishing Group |
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| Online Access | Get full text |
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| Abstract | Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant.
The Omicron variant evades vaccine-induced neutralization but also fails to form syncytia, shows reduced replication in human lung cells and preferentially uses a TMPRSS2-independent cell entry pathway, which may contribute to enhanced replication in cells of the upper airway. Altered fusion and cell entry characteristics are linked to distinct regions of the Omicron spike protein. |
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| AbstractList | Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant. Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant. The Omicron variant evades vaccine-induced neutralization but also fails to form syncytia, shows reduced replication in human lung cells and preferentially uses a TMPRSS2-independent cell entry pathway, which may contribute to enhanced replication in cells of the upper airway. Altered fusion and cell entry characteristics are linked to distinct regions of the Omicron spike protein. Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant.Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant. Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant.The Omicron variant evades vaccine-induced neutralization but also fails to form syncytia, shows reduced replication in human lung cells and preferentially uses a TMPRSS2-independent cell entry pathway, which may contribute to enhanced replication in cells of the upper airway. Altered fusion and cell entry characteristics are linked to distinct regions of the Omicron spike protein. |
| Author | Furnon, Wilhelm Smollett, Katherine Scott, Sam Szemiel, Agnieszka Vink, Elen Pascall, David J. Orton, Richard Murcia, Pablo R. Silva, Vanessa Klenerman, Paul Tong, Lily Haughney, John Harvey, William T. Manali, Maria Holden, Matthew T. G. Robertson, David L. MacLean, Oscar A. Holland, Poppy Pinto, Rute Maria Wilkie, Craig Templeton, Kate Thomson, Emma C. Asamaphan, Patawee Palmarini, Massimo da Silva Filipe, Ana Patel, Arvind H. Ray, Surajit Gunson, Rory Shaaban, Sharif Hughes, Joseph Cantoni, Diego Puxty, Kathryn Logan, Nicola Grove, Joe De Lorenzo, Giuditta Ashraf, Shirin Dunachie, Susanna Davis, Chris Cowton, Vanessa Yebra, Gonzalo Willett, Brian J. |
| Author_xml | – sequence: 1 givenname: Brian J. orcidid: 0000-0001-8912-3266 surname: Willett fullname: Willett, Brian J. email: brian.willett@glasgow.ac.uk organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 2 givenname: Joe orcidid: 0000-0001-5390-7579 surname: Grove fullname: Grove, Joe email: joe.grove@glasgow.ac.uk organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 3 givenname: Oscar A. surname: MacLean fullname: MacLean, Oscar A. organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 4 givenname: Craig orcidid: 0000-0003-0805-0195 surname: Wilkie fullname: Wilkie, Craig organization: School of Mathematics & Statistics, University of Glasgow – sequence: 5 givenname: Giuditta orcidid: 0000-0002-2736-8740 surname: De Lorenzo fullname: De Lorenzo, Giuditta organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 6 givenname: Wilhelm orcidid: 0000-0002-5588-4232 surname: Furnon fullname: Furnon, Wilhelm organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 7 givenname: Diego surname: Cantoni fullname: Cantoni, Diego organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 8 givenname: Sam orcidid: 0000-0001-7080-8038 surname: Scott fullname: Scott, Sam organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 9 givenname: Nicola surname: Logan fullname: Logan, Nicola organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 10 givenname: Shirin orcidid: 0000-0002-6468-0258 surname: Ashraf fullname: Ashraf, Shirin organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 11 givenname: Maria surname: Manali fullname: Manali, Maria organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 12 givenname: Agnieszka surname: Szemiel fullname: Szemiel, Agnieszka organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 13 givenname: Vanessa orcidid: 0000-0003-1813-7825 surname: Cowton fullname: Cowton, Vanessa organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 14 givenname: Elen orcidid: 0000-0001-8535-6214 surname: Vink fullname: Vink, Elen organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 15 givenname: William T. surname: Harvey fullname: Harvey, William T. organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 16 givenname: Chris surname: Davis fullname: Davis, Chris organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 17 givenname: Patawee surname: Asamaphan fullname: Asamaphan, Patawee organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 18 givenname: Katherine surname: Smollett fullname: Smollett, Katherine organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 19 givenname: Lily orcidid: 0000-0003-3882-3339 surname: Tong fullname: Tong, Lily organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 20 givenname: Richard surname: Orton fullname: Orton, Richard organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 21 givenname: Joseph orcidid: 0000-0003-2556-2563 surname: Hughes fullname: Hughes, Joseph organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 22 givenname: Poppy orcidid: 0000-0001-9708-9555 surname: Holland fullname: Holland, Poppy organization: NHS Greater Glasgow & Clyde – sequence: 23 givenname: Vanessa surname: Silva fullname: Silva, Vanessa organization: NHS Greater Glasgow & Clyde – sequence: 24 givenname: David J. orcidid: 0000-0002-7543-0860 surname: Pascall fullname: Pascall, David J. organization: MRC Biostatistics Unit, University of Cambridge – sequence: 25 givenname: Kathryn orcidid: 0000-0002-5742-6171 surname: Puxty fullname: Puxty, Kathryn organization: NHS Greater Glasgow & Clyde – sequence: 26 givenname: Ana orcidid: 0000-0002-9442-2903 surname: da Silva Filipe fullname: da Silva Filipe, Ana organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 27 givenname: Gonzalo orcidid: 0000-0002-3472-3667 surname: Yebra fullname: Yebra, Gonzalo organization: Public Health Scotland – sequence: 28 givenname: Sharif surname: Shaaban fullname: Shaaban, Sharif organization: Public Health Scotland – sequence: 29 givenname: Matthew T. G. surname: Holden fullname: Holden, Matthew T. G. organization: Public Health Scotland, School of Medicine, University of St Andrews – sequence: 30 givenname: Rute Maria surname: Pinto fullname: Pinto, Rute Maria organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 31 givenname: Rory surname: Gunson fullname: Gunson, Rory organization: NHS Greater Glasgow & Clyde – sequence: 32 givenname: Kate surname: Templeton fullname: Templeton, Kate organization: NHS Lothian – sequence: 33 givenname: Pablo R. orcidid: 0000-0002-4352-394X surname: Murcia fullname: Murcia, Pablo R. organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 34 givenname: Arvind H. orcidid: 0000-0003-4600-2047 surname: Patel fullname: Patel, Arvind H. organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 35 givenname: Paul surname: Klenerman fullname: Klenerman, Paul organization: University of Oxford – sequence: 36 givenname: Susanna orcidid: 0000-0001-5665-6293 surname: Dunachie fullname: Dunachie, Susanna organization: University of Oxford – sequence: 39 givenname: John surname: Haughney fullname: Haughney, John organization: NHS Greater Glasgow & Clyde – sequence: 40 givenname: David L. orcidid: 0000-0001-6338-0221 surname: Robertson fullname: Robertson, David L. organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 41 givenname: Massimo surname: Palmarini fullname: Palmarini, Massimo organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow – sequence: 42 givenname: Surajit orcidid: 0000-0003-3965-8136 surname: Ray fullname: Ray, Surajit organization: School of Mathematics & Statistics, University of Glasgow – sequence: 43 givenname: Emma C. orcidid: 0000-0003-1482-0889 surname: Thomson fullname: Thomson, Emma C. email: emma.thomson@glasgow.ac.uk organization: MRC-University of Glasgow Centre for Virus Research, University of Glasgow, NHS Greater Glasgow & Clyde, London School of Hygiene and Tropical Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35798890$$D View this record in MEDLINE/PubMed |
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| Contributor | Munn, Robert Merrick, Ian McMurray, Claire L Menegazzo, Mirko Fleming, Vicki M Spellman, Karla Boswell, Tim Morriss, Arthur Clark, Gemma Blakey, Victoria Joseph, Amelia Workman, Trudy Brown, Anthony Adams, Helen Abudahab, Khalil Murray, Abigail Underwood, Anthony P Barnes, Eleanor Berry, Louise Holmes, Christopher W Buchan, Sarah L Afifi, Safiah Duncan, Christopher Adele, Sandra Turtle, Lance Moore, Shona Patel, Amita Nebbia, Gaia Beer, Robert Klenerman, Paul de Silva, Thushan Snell, Luke B Mantzouratou, Anna Raviprakash, Veena Robson, Samuel C Beckwith, Shaun M Abraham, Priyanka Willford, Nicholas J Jones, Owen Reynolds, Nicola Shaw, Jessica Deeks, Alexandra Morgan, Sian Edgeworth, Jonathan Campbell, Sharon McKenna, James P Kitchen, Christine Odedra, Mina Bird, Paul W Marchbank, Angela Patel, Bindi Fallon, Karlie Price, Anna Thomson, Laura Fryer, Helen John, Michaela Whalley, Thomas Charalampous, Themoula Murray, Sam M Guest, Martyn Kele, Beatrix Batra, Rahul Sheriff, Nicola Shelest, Ekaterina Barrow, Magdalena Williams, Lesley-Anne Mack, Andrew Payn |
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| Copyright | The Author(s) 2022. corrected publication 2022 2022. The Author(s). The Author(s) 2022. corrected publication 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Author(s) 2022, corrected publication 2022 |
| Copyright_xml | – notice: The Author(s) 2022. corrected publication 2022 – notice: 2022. The Author(s). – notice: The Author(s) 2022. corrected publication 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: The Author(s) 2022, corrected publication 2022 |
| CorporateAuthor | PITCH Consortium The COVID-19 Genomics UK (COG-UK) Consortium COVID-19 Genomics UK (COG-UK) Consortium |
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| Title | SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway |
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