Evidence map›Paper›PMID 37565297›Full record

ArticleClinical and experimental immunology2023

Soluble wild-type ACE2 molecules inhibit newer SARS-CoV-2 variants and are a potential antiviral strategy to mitigate disease severity in COVID-19.

Rohan Ameratunga, Emily Mears, Euphemia Leung, Russell Snell, See-Tarn Woon, William Kelton, Natalie Medlicott, Anthony Jordan, William Abbott, Richard Steele and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

13 authors at 5 institutions in 1 country.

Rohan AmeratungaDepartment of Clinical immunology, Auckland Hospital, AucklandNew Zealand.ORCID 0000-0002-3011-8654
Emily MearsApplied Translational Genetic Group, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Euphemia LeungAuckland Cancer Society Research Centre, School of Medical Sciences, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Russell SnellApplied Translational Genetic Group, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
See-Tarn WoonDepartment of Virology and Immunology, Auckland Hospital, Auckland, New Zealand.
William KeltonTe Huataki Waiora School of Health, University of Waikato, Hamilton, New Zealand.
Natalie MedlicottSchool of Pharmacy, University of Otago, Dunedin, New Zealand.
Anthony JordanDepartment of Clinical immunology, Auckland Hospital, AucklandNew Zealand.
William AbbottDepartment of Surgery, Auckland Hospital, Auckland, New Zealand.
Richard SteeleDepartment of Respiratory Medicine, Wellington Hospital, Wellington, New Zealand.
William RollestonSouth Pacific Sera, Timaru, New Zealand.
Hilary LonghurstDepartment of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.
Klaus LehnertApplied Translational Genetic Group, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
University of Auckland · NZAuckland City Hospital · NZUniversity of Otago · NZUniversity of Waikato · NZWellington Hospital · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease of 2019 (COVID-19), has caused havoc around the world. While several COVID-19 vaccines and drugs have been authorized for use, these antiviral drugs remain beyond the reach of most low- and middle-income countries. Rapid viral evolution is reducing the efficacy of vaccines and monoclonal antibodies and contributing to the deaths of some fully vaccinated persons. Others with normal immunity may have chosen not to be vaccinated and remain at risk if they contract the infection. Vaccines may not protect some immunodeficient patients from SARS-CoV-2, who are also at increased risk of chronic COVID-19 infection, a dangerous stalemate between the virus and a suboptimal immune response. Intra-host viral evolution could rapidly lead to the selection and dominance of vaccine and monoclonal antibody-resistant clades of SARS-CoV-2. There is thus an urgent need to develop new treatments for COVID-19. The NZACE2-Pātari project, comprising modified soluble angiotensin-converting enzyme 2 (ACE2) molecules, seeks to intercept and block SARS-CoV-2 infection of the respiratory mucosa. In vitro data presented here show that soluble wild-type ACE2 molecules retain the ability to effectively block the Spike (S) glycoprotein of SARS-CoV-2 variants including the ancestral Wuhan, delta (B.1.617.2) and omicron (B.1.1.529) strains. This therapeutic strategy may prove effective if implemented early during the nasal phase of the infection and may act synergistically with other antiviral drugs such as Paxlovid to further mitigate disease severity.

Indexed as

COVID-19SARS-CoV-2Angiotensin-Converting Enzyme 2Antiviral AgentsCOVID-19 VaccinesHumansPatient AcuityPeptidyl-Dipeptidase AAngiotensin-Converting Enzyme 2Antiviral AgentsCOVID-19 VaccinesPeptidyl-Dipeptidase AACE2antiviralCOVID-19mucosal therapySARS-CoV-2vaccines

Identifiers

PMID37565297
PMCPMC10719217
OpenAlexW4385752246

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.