Evidence map›Paper›PMID 33740397›Full record

ArticleCell systems2021

Modeling the complete kinetics of coxsackievirus B3 reveals human determinants of host-cell feedback.

Aaron B Lopacinski, Andrew J Sweatt, Christian M Smolko, Elise Gray-Gaillard, Cheryl A Borgman, Millie Shah, Kevin A Janes

Open access · bronzeAbstract read
In one paragraph

Article in Cell systems, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Systems Virology at Scale.Current opinion in systems biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Three Modes of Viral Adaption by the Heart.bioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Aaron B LopacinskiDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Andrew J SweattDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Christian M SmolkoDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Elise Gray-GaillardDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21231, USA.
Cheryl A BorgmanDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Millie ShahDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: ms2kf@virginia.edu.
Kevin A JanesDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA; Department of Biochemistry & Molecular Genetics, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: kjanes@virginia.edu.
University of Virginia · US

Funding

BASIC CARDIOVASCULAR RESEARCH TRAINING GRANTT32HL007284 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Brant E Isakson, Gary K Owens · 1985 to 2026
$19.6M
NHLBI NIH HHS T32 HL007284
6 · The paper itself

Abstract

Complete kinetic models are pervasive in chemistry but lacking in biological systems. We encoded the complete kinetics of infection for coxsackievirus B3 (CVB3), a compact and fast-acting RNA virus. The model consists of separable, detailed modules describing viral binding-delivery, translation-replication, and encapsidation. Specific module activities are dampened by the type I interferon response to viral double-stranded RNAs (dsRNAs), which is itself disrupted by viral proteinases. The experimentally validated kinetics uncovered that cleavability of the dsRNA transducer mitochondrial antiviral signaling protein (MAVS) becomes a stronger determinant of viral outcomes when cells receive supplemental interferon after infection. Cleavability is naturally altered in humans by a common MAVS polymorphism, which removes a proteinase-targeted site but paradoxically elevates CVB3 infectivity. These observations are reconciled with a simple nonlinear model of MAVS regulation. Modeling complete kinetics is an attainable goal for small, rapidly infecting viruses and perhaps viral pathogens more broadly. A record of this paper's transparent peer review process is included in the Supplemental information.

Indexed as

Enterovirus B, HumanHost-Pathogen InteractionsHumansKineticsantiviralenterovirusflaviviruspicornaviruspoliovirusreplication organelle

Identifiers

PMID33740397
PMCPMC8112228
OpenAlexW3138473175

What OpenQuestion holds

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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.