Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant
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Emergence of SARS-CoV-2 variants, including the globally successful B.1.1.7 lineage, suggests viral adaptations to host selective pressures resulting in more efficient transmission. Although much effort has focused on Spike adaptation for viral entry and adaptive immune escape, B.1.1.7 mutations outside Spike likely contribute to enhance transmission. Here we used unbiased abundance proteomics, phosphoproteomics, mRNA sequencing and viral replication assays to show that B.1.1.7 isolates more effectively suppress host innate immune responses in airway epithelial cells. We found that B.1.1.7 isolates have dramatically increased subgenomic RNA and protein levels of Orf9b and Orf6, both known innate immune antagonists. Expression of Orf9b alone suppressed the innate immune response through interaction with TOM70, a mitochondrial protein required for RNA sensing adaptor MAVS activation, and Orf9b binding and activity was regulated via phosphorylation. We conclude that B.1.1.7 has evolved beyond the Spike coding region to more effectively antagonise host innate immune responses through upregulation of specific subgenomic RNA synthesis and increased protein expression of key innate immune antagonists. We propose that more effective innate immune antagonism increases the likelihood of successful B.1.1.7 transmission, and may increase in vivo replication and duration of infection.
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The Alpha variant contains non-spike mutations including nsp6:Δ106-108 and nucleocapsid mutations D3L, R203K and G204R, which may increase transmission by antagonizing innate immunity.
“The Alpha variant also contains several non-spike mutations including nsp6:Δ106-108 and the nucleocapsid mutations D3L, R203K and G204R, which may increase transmission by antagonizing innate immunity 25,[185][186][187] .”
From The biological and clinical significance of emerging SARS-CoV-2 variants (2021) · cites this paper as [185]
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How a rampant coronavirus variant blunts our immune defences
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- Authors
- Thorne, L. G., Bouhaddou, M., Reuschl, A.-K., Zuliani-Alvarez, L., Polacco, B., Pelin, A., Batra, J., Whelan, M. V. X., Ummadi, M., Rojc, A., Turner, J., Obernier, K., Braberg, H., Soucheray, M., Richards, A., Chen, K.-H., Harjai, B., Memon, D., Hosmillo, M., Hiatt, J., Jahun, A., Goodfellow, I. G., Fabius, J. M., Shokat, K., Jura, N., Verba, K., Noursadeghi, M., Beltrao, P., Swaney, D. L., Garcia-Sastre, A., Jolly, C., Towers, G. J., & Krogan, N. J.
- Affiliations
- University College London (GB)
- Gladstone Institutes (US)
- European Bioinformatics Institute (GB)
- University of Cambridge (GB)
- University of California, San Francisco (US)
- Corresponding author
- Jolly, Clare
- Towers, Greg J.
- Krogan, Nevan J.
- ORCID
- Thorne, Lucy G
- Bouhaddou, Mehdi
- Reuschl, Ann-Kathrin
- Zuliani-Alvarez, Lorena
- Polacco, Ben
- Pelin, Adrian
- Batra, Jyoti
- Whelan, Matthew V.X.
- Ummadi, Manisha
- Rojc, Ajda
- Turner, Jane
- Obernier, Kirsten
- Braberg, Hannes
- Soucheray, Margaret
- Richards, Alicia
- Chen, Kuei-Ho
- Memon, Danish
- Hosmillo, Myra
- Hiatt, Joseph
- Jahun, Aminu
- Goodfellow, Ian G.
- Shokat, Kevan
- Jura, Natalia
- Verba, Klim
- Noursadeghi, Mahdad
- Beltrao, Pedro
- Swaney, Danielle L.
- Garcia-Sastre, Adolfo
- Jolly, Clare
- Towers, Greg J.
- Krogan, Nevan J.
- Venue
- bioRxiv (Cold Spring Harbor Laboratory)
- Publisher
- openRxiv
- Published
- 2021-06-07
- PMC
- PMC8202424
- OpenAlex
- W3168293628
- Cited by
- 91
- References
- 66
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 5 · 2022: 39 · 2021: 41 · 2020: 1
- Type
- posted content
- Language
- en
- Open access
- green
- doi.org
- Licence
- cc-by
- Locations
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion, cc-by)
- Funders
- U.S. Department of Defense (75N93021C00014)
- F. Hoffmann-La Roche
- Roddenberry Foundation
- Wellcome Trust (220863, MR/W005611/1, 108079, 207498, 206298, 207511, 108183, 200927)
- UK Research and Innovation (MR/W005611/1/)
- Open Philanthropy Project (#2020-215611, HHSN272201400008C)
- National Institute for Health Research Health Protection Research Unit (200927, 207498)
- National Institute for Health and Care Research (207498, 200 927)
- Imperial College London (200927)
- Public Health England (200927)
- University College London Hospitals NHS Foundation Trust
- National Institutes of Health (HR0011-19-2-0020, 75N93021C00014, COVID-19, HHSN272201400008C, 133122P, P50AI150476, U19AI135990, U19AI135972, R01AI143292, R01AI120694, and P01AI063302)
- Defense Advanced Research Projects Agency (HR0011, HR0011-19-2-0020, U19AI135972)
- University of California, San Francisco
- Advanced Research Projects Agency
- Medical Research Council (MR/W005611/1)
- National Cancer Institute (F32CA239333, 75N93021C00014, U54CA260560)
- National Institute of General Medical Sciences (T32GM007618, R01GM133981)
- National Institute of Allergy and Infectious Diseases (HHSN272201400008C), #75N93021C00014, R01AI120694, R01AI143292, P50AI150476, contract # 75N93021C00014, 2020-215611, U19AI135990, P01AI063302, U19AI135972)
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Keywords
- SARS-CoV-2, B.1.1.7 variant, Omicron variant, innate immune evasion, ORF9b, ORF6, Tom70, MAVS, subgenomic RNA, airway epithelial cells, virus transmission, host-virus interaction, protein phosphorylation, viral evolution
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