Evidence map›Paper›PMID 18032498›Full record

ArticleJournal of virology2008

Amino acid substitutions in the S2 subunit of mouse hepatitis virus variant V51 encode determinants of host range expansion.

Willie C McRoy, Ralph S Baric

Abstract 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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Patterns of Recombination in Coronaviruses.International journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. The coronavirus recombination pathway.Cell host & microbe · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Studying Evolutionary Adaptation of MERS-CoV.Methods in molecular biology (Clifton, N.J.) · 2020
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Molecular aspects of MERS-CoV.Frontiers of medicine · 2017
    Review
  17. Retroviral host range extension is coupled with Env-activating mutations resulting in receptor-independent entry.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Review
  19. Article
  20. SARS-like WIV1-CoV poised for human emergence.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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

2 authors.

Willie C McRoyUniversity of North Carolina at Chapel Hill, 2107 McGavran Greenberg Hall, CB 7435, Chapel Hill, NC 27599-7435, USA.
Ralph S Baric

Funding

Molecular Biology of Viral Diseases Predoctoral Training GrantT32AI007419 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Mark T Heise, CARY A MOODY · 1993 to 2026
$4.7M
STUDIES INTO THE MECHANISMS FOR MHV REPLICATIONR01AI023946 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BARIC, RALPH S · 1986 to 2007
$2.3M
NIAID NIH HHS AI07419-13NIAID NIH HHS AI23946-15NIAID NIH HHS R01 AI023946NIAID NIH HHS T32 AI007419
6 · The paper itself

Abstract

We previously described mouse hepatitis virus (MHV) variant V51 derived from a persistent infection of murine DBT cells with an expanded host range (R. S. Baric, E. Sullivan, L. Hensley, B. Yount, and W. Chen, J. Virol. 73:638-649, 1999). Sequencing of the V51 spike gene, the mediator of virus entry, revealed 13 amino acid substitutions relative to the originating MHV A59 strain. Seven substitutions were located in the amino-terminal S1 cleavage subunit, and six were located in the carboxy-terminal S2 cleavage subunit. Using targeted RNA recombination, we constructed a panel of recombinant viruses to map the mediators of host range to the six substitutions in S2, with a subgroup of four changes of particular interest. This subgroup maps to two previously identified domains within S2, a putative fusion peptide and a heptad repeat, both conserved features of class I fusion proteins. In addition to an altered host range, V51 displayed altered utilization of CEACAM1a, the high-affinity receptor for A59. Interestingly, a recombinant with S1 from A59 and S2 from V51 was severely debilitated in its ability to productively infect cells via CEACAM1a, while the inverse recombinant was not. This result suggests that the S2 substitutions exert powerful effects on the fusion trigger that normally passes from S1 to S2. These novel findings play against the existing data that suggest that MHV host range determinants are located in the S1 subunit, which harbors the receptor binding domain, or involve coordinating changes in both S1 and S2. Mounting evidence also suggests that the class I fusion mechanism may possess some innate plasticity that regulates viral host range.

Indexed as

Virus InternalizationAmino Acid SubstitutionAnimalsCarcinoembryonic AntigenCatsCell LineCricetinaeCricetulusHumansMembrane GlycoproteinsMiceMurine hepatitis virusSpike Glycoprotein, CoronavirusSwineViral Envelope ProteinsCarcinoembryonic AntigenCeacam1 protein, mouseMembrane GlycoproteinsSpike Glycoprotein, CoronavirusViral Envelope Proteins

Identifiers

PMID18032498
PMCPMC2224421

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Registered trials

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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.