ArticlebioRxiv : the preprint server for biology2021
Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant.
Article in bioRxiv : the preprint server for biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 106 citations in OpenAlex.
- Review
- SARS-CoV-2 variant Alpha has a spike-dependent replication advantage over the ancestral B.1 strain in human cells with low ACE2 expression.PLoS biology · 2022Article
- Pathogen evolution during vaccination campaigns.PLoS biology · 2022Article
- Human coronaviruses disassemble processing bodies.PLoS pathogens · 2022Article
- Advances and gaps in SARS-CoV-2 infection models.PLoS pathogens · 2022Review
- The biological and clinical significance of emerging SARS-CoV-2 variants.Nature reviews. Genetics · 2021Review
- S-farnesylation is essential for antiviral activity of the long ZAP isoform against RNA viruses with diverse replication strategies.PLoS pathogens · 2021Article
- TOM70 in Glial Cells as a Potential Target for Treatment of COVID-19.Frontiers in cellular neuroscience · 2021Article
- Innate Immunity Evasion Strategies of Highly Pathogenic Coronaviruses: SARS-CoV, MERS-CoV, and SARS-CoV-2.Frontiers in microbiology · 2021Review
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Authors and funding
33 authors at 6 institutions in 2 countries.
Funding
Abstract
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
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.