Evidence map›Paper›PMID 32659783›Full record

ArticleNature2020

A perspective on potential antibody-dependent enhancement of SARS-CoV-2.

Ann M Arvin, Katja Fink, Michael A Schmid, Andrea Cathcart, Roberto Spreafico, Colin Havenar-Daughton, Antonio Lanzavecchia, Davide Corti, Herbert W Virgin

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Nature, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
305citing papers in PubMed, 2 pooled it
12.3field-weighted citation impact, top 1% 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

305 citing papers in PubMed, 2 syntheses or guidelines pooled it, 533 citations in OpenAlex.

  1. Pooled it
  2. SARS-CoV-2-neutralising monoclonal antibodies for treatment of COVID-19.The Cochrane database of systematic reviews · 2021
    Pooled it
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245 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Ann M ArvinVir Biotechnology, San Francisco, CA, USA. aarvin@vir.bio.
Katja FinkVir Biotechnology, San Francisco, CA, USA.
Michael A SchmidVir Biotechnology, San Francisco, CA, USA.
Andrea CathcartVir Biotechnology, San Francisco, CA, USA.
Roberto SpreaficoVir Biotechnology, San Francisco, CA, USA.
Colin Havenar-DaughtonVir Biotechnology, San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-2880-3927
Antonio LanzavecchiaVir Biotechnology, San Francisco, CA, USA.
Davide CortiVir Biotechnology, San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-5797-1364
Herbert W VirginVir Biotechnology, San Francisco, CA, USA. svirgin@vir.bio.ORCID http://orcid.org/0000-0001-8580-7628
Vir Biotechnology (Switzerland) · CHVIR Biotechnology (United States) · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibody-dependent enhancement (ADE) of disease is a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we review observations relevant to the risks of ADE of disease, and their potential implications for SARS-CoV-2 infection. At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies-regardless of what virus is the causative agent-it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward.

Indexed as

AnimalsAntibodies, NeutralizingAntibodies, ViralAntibody-Dependent EnhancementBetacoronavirusCoronavirus InfectionsCOVID-19COVID-19 VaccinesDengue VirusDisease Models, AnimalHEK293 CellsHumansImmunoglobulin Fab FragmentsImmunoglobulin Fc FragmentsImmunoglobulin GMacaca mulattaAntibodies, NeutralizingAntibodies, ViralCOVID-19 VaccinesImmunoglobulin Fab FragmentsImmunoglobulin Fc FragmentsImmunoglobulin GViral Vaccines

Identifiers

PMID32659783
OpenAlexW3040725637

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.