Evidence map›Paper›PMID 33836527›Full record

ArticleILAR journal2021

Animal Models of COVID-19. I. Comparative Virology and Disease Pathogenesis.

Caroline J Zeiss, Susan Compton, Rebecca Terilli Veenhuis

Open access · hybridAbstract read
In one paragraph

Article in ILAR journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. SARS-CoV-2 Infection and Lung Regeneration.Clinical microbiology reviews · 2022
    Review
  10. Article
  11. Central nervous system outcomes of COVID-19.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  12. Review
  13. UsingExpert opinion on drug discovery · 2022
    Article
  14. Article
  15. Article
  16. 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

3 authors at 3 institutions in 1 country.

Caroline J ZeissDepartment of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Susan ComptonDepartment of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
Rebecca Terilli VeenhuisDepartment of Comparative Medicine, John Hopkins School of Medicine, Baltimore, Maryland, USA.
University of Maryland, Baltimore · USUniversity of New Haven · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
NCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

The Coronavirus Disease 2019 (COVID-19) pandemic has fueled unprecedented development of animal models to understand disease pathogenesis, test therapeutics, and support vaccine development. Models previously developed to study severe acute respiratory syndrome coronavirus (SARS-CoV) have been rapidly deployed to study SARS-CoV-2. However, it has become clear that despite the common use of ACE2 as a receptor for both viruses, the host range of the 2 viruses does not entirely overlap. Distinct ACE2-interacting residues within the receptor binding domain of SARS-CoV and SARS-CoV-2, as well as species differences in additional proteases needed for activation and internalization of the virus, are likely sources of host differences between the 2 viruses. Spontaneous models include rhesus and cynomolgus macaques, African Green monkeys, hamsters, and ferrets. Viral shedding and transmission studies are more frequently reported in spontaneous models. Mice can be infected with SARS-CoV; however, mouse and rat ACE2 does not support SARS-CoV-2 infection. Murine models for COVID-19 are induced through genetic adaptation of SARS-CoV-2, creation of chimeric SARS-CoV and SARS-CoV-2 viruses, use of human ACE2 knock-in and transgenic mice, and viral transfection of wild-type mice with human ACE2. Core aspects of COVID-19 are faithfully reproduced across species and model. These include the acute nature and predominantly respiratory source of viral shedding, acute transient and nonfatal disease with a largely pulmonary phenotype, similar short-term immune responses, and age-enhanced disease. Severity of disease and tissue involvement (particularly brain) in transgenic mice varies by promoter. To date, these models have provided a remarkably consistent template on which to test therapeutics, understand immune responses, and test vaccine approaches. The role of comorbidity in disease severity and the range of severe organ-specific pathology in humans remains to be accurately modeled.

Indexed as

COVID-19Severe acute respiratory syndrome-related coronavirusAngiotensin-Converting Enzyme 2AnimalsChlorocebus aethiopsCricetinaeDisease Models, AnimalFerretsMiceMice, TransgenicModels, AnimalPeptidyl-Dipeptidase ARatsReceptors, VirusSARS-CoV-2Angiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AReceptors, Virus

Identifiers

PMID33836527
PMCPMC8083356
OpenAlexW3150233706

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.