Evidence map›Paper›PMID 18094188›Full record

ArticleJournal of virology2008

Mechanisms of zoonotic severe acute respiratory syndrome coronavirus host range expansion in human airway epithelium.

Timothy Sheahan, Barry Rockx, Eric Donaldson, Amy Sims, Raymond Pickles, Davide Corti, Ralph Baric

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

88 citing papers in PubMed, 137 citations in OpenAlex.

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  12. Immunology and controlling of coronaviruses; the current enemy for humanity: A review.International journal of biological macromolecules · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Molecular Basis of the Therapeutical Potential of Clove (Molecules (Basel, Switzerland) · 2021
    Review
  17. Review
  18. Review
  19. Article
  20. Review

28 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

7 authors at 1 institution in 1 country.

Timothy SheahanDepartment of Epidemiology, 2107 McGavran-Greenberg, CB#7435, University of North Carolina, Chapel Hill, NC 27699-7435, USA.
Barry Rockx
Eric Donaldson
Amy Sims
Raymond Pickles
Davide Corti
Ralph Baric
University of North Carolina at Chapel Hill · US

Funding

SARS Replicase Proteins in Pathogenesis and ReplicationP01AI059443 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 2005 to 2009
$9.2M
SARS Reverse GeneticsR01AI059136 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 2004 to 2008
$1.4M
NIAID NIH HHS AI059443NIAID NIH HHS P01 AI059443NIAID NIH HHS R01 AI059136
6 · The paper itself

Abstract

In 2003, severe acute respiratory syndrome coronavirus (SARS-CoV) emerged and caused over 8,000 human cases of infection and more than 700 deaths worldwide. Zoonotic SARS-CoV likely evolved to infect humans by a series of transmission events between humans and animals for sale in China. Using synthetic biology, we engineered the spike protein (S) from a civet strain, SZ16, into our epidemic strain infectious clone, creating the chimeric virus icSZ16-S, which was infectious but yielded progeny viruses incapable of propagating in vitro. After introducing a K479N mutation within the S receptor binding domain (RBD) of SZ16, the recombinant virus (icSZ16-S K479N) replicated in Vero cells but was severely debilitated in growth. The in vitro evolution of icSZ16-S K479N on human airway epithelial (HAE) cells produced two viruses (icSZ16-S K479N D8 and D22) with enhanced growth on HAE cells and on delayed brain tumor cells expressing the SARS-CoV receptor, human angiotensin I converting enzyme 2 (hACE2). The icSZ16-S K479N D8 and D22 virus RBDs contained mutations in ACE2 contact residues, Y442F and L472F, that remodeled S interactions with hACE2. Further, these viruses were neutralized by a human monoclonal antibody (MAb), S230.15, but the parent icSZ16-S K479N strain was eight times more resistant than the mutants. These data suggest that the human adaptation of zoonotic SARS-CoV strains may select for some variants that are highly susceptible to select MAbs that bind to RBDs. The epidemic, icSZ16-S K479N, and icSZ16-S K479N D22 viruses replicate similarly in the BALB/c mouse lung, highlighting the potential use of these zoonotic spike SARS-CoVs to assess vaccine or serotherapy efficacy in vivo.

Indexed as

ZoonosesAmino Acid SequenceAnimalsBase SequenceChlorocebus aethiopsDNA PrimersEpithelial CellsHumansImmunohistochemistryMembrane GlycoproteinsMiceMice, Inbred BALB CMolecular Sequence DataPhylogenyReverse Transcriptase Polymerase Chain ReactionSevere acute respiratory syndrome-related coronavirusDNA PrimersMembrane GlycoproteinsSpike Glycoprotein, CoronavirusViral Envelope Proteins

Identifiers

PMID18094188
PMCPMC2258931
OpenAlexW2099851748

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.