Evidence map›Paper›PMID 32795830›Full record

ArticleMedical hypotheses2020

Autoimmunity to ACE2 as a possible cause of tissue inflammation in Covid-19.

Alain Townsend

Open access · hybridAbstract read
In one paragraph

Article in Medical hypotheses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 27% of its field
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

7 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Alain TownsendHuman Immunology Unit, Weatherall Institute, Oxford OX39DS, United Kingdom. Electronic address: Alain.townsend@imm.ox.ac.uk.
MRC Human Immunology Unit · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

hypothesisThe delayed lung damage after SARS-CoV-2 infection may be caused by an autoimmune response to ACE2 induced by forced presentation of the ACE2 protein in a complex with CoV Spike in Fc Receptor positive Antigen Presenting Cells in the lung. The likelihood that this hypothesis is valid is low, but it is easily tested. TESTABLE PREDICTIONS: 1) Autoantibodies and T cells to ACE2 may be found in patients with the lung damage but not in those without 2) There may be an HLA linkage with the delayed lung disease 3) Vaccines based on the spike protein might initiate the process by amplifying Fc mediated uptake of ACE2-Spike complexes into APCs. PRACTICAL IMPLICATIONS: The development of autoantibodies to ACE2 might predict the development of the inflammatory phase of Covid-19 disease. It might be wise to consider engineering versions of the spike that no longer bind to ACE2 for inclusion in vaccines.

Indexed as

AutoimmunityAngiotensin-Converting Enzyme 2Antigen-Presenting CellsAutoantibodiesBinding SitesCOVID-19HLA AntigensHumansInflammationLung DiseasesModels, TheoreticalProtein BindingProtein DomainsReceptors, FcSpike Glycoprotein, CoronavirusT-LymphocytesACE2 protein, humanAngiotensin-Converting Enzyme 2AutoantibodiesHLA AntigensReceptors, FcSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2

Identifiers

PMID32795830
PMCPMC7382330
OpenAlexW3044653813

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.