Evidence map›Paper›PMID 33851153›Full record

ArticlebioRxiv : the preprint server for biology2021

Functional evaluation of the P681H mutation on the proteolytic activation the SARS-CoV-2 variant B.1.1.7 (Alpha) spike.

Bailey Lubinski, Maureen H V Fernandes, Laura Frazier, Tiffany Tang, Susan Daniel, Diego G Diel, Javier A Jaimes, Gary R Whittaker

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 71 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Bailey LubinskiDepartment of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Maureen H V FernandesDepartment of Population Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Laura FrazierDepartment of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Tiffany TangRobert Frederick Smith School of Chemical & Biomolecular Engineering, Cornell University, Ithaca, NY, 14853, USA.
Susan DanielRobert Frederick Smith School of Chemical & Biomolecular Engineering, Cornell University, Ithaca, NY, 14853, USA.
Diego G DielDepartment of Population Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Javier A JaimesDepartment of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Gary R WhittakerDepartment of Microbiology & Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA.
Cornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent causing the COVID-19 pandemic. SARS-CoV-2 B.1.1.7 (Alpha), a WHO variant of concern (VOC) first identified in the UK in late 2020, contains several mutations including P681H in the spike S1/S2 cleavage site, which is predicted to increase cleavage by furin, potentially impacting the viral cell entry. Here, we studied the role of the P681H mutation in B.1.1.7 cell entry. We performed assays using fluorogenic peptides mimicking the Wuhan-Hu-1 and B.1.1.7 S1/S2 sequence and observed no significant difference in furin cleavage. Functional assays using pseudoparticles harboring SARS-CoV-2 spikes and cell-to-cell fusion assays demonstrated no differences between Wuhan-Hu-1, B.1.1.7 or a P681H point mutant. Likewise, we observed no differences in viral growth between USA-WA1/2020 and a B.1.1.7 isolate in cell culture. Our findings suggest that while the B.1.1.7 P681H mutation may slightly increase S1/S2 cleavage this does not significantly impact viral entry or cell-cell spread.

Identifiers

PMID33851153
PMCPMC8043443
OpenAlexW3147586498

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.