Evidence map›Paper›PMID 21156827›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Transfer of a prion strain to different hosts leads to emergence of strain variants.

Sukhvir P Mahal, Shawn Browning, Jiali Li, Irena Suponitsky-Kroyter, Charles Weissmann

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. The role of prion strain diversity in the development of successful therapeutic treatments.Progress in molecular biology and translational science · 2020
    Review
  6. Synthetic Prion Selection and Adaptation.Molecular neurobiology · 2019
    Article
  7. Cellular and Molecular Mechanisms of Prion Disease.Annual review of pathology · 2019
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Biology and Genetics of PrP Prion Strains.Cold Spring Harbor perspectives in medicine · 2017
    Review
  13. Prion Strain Diversity.Cold Spring Harbor perspectives in medicine · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Prions are affected by evolution at two levels.Cellular and molecular life sciences : CMLS · 2016
    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

5 authors at 3 institutions in 1 country.

Sukhvir P MahalDepartment of Infectology, Scripps Florida, Jupiter, FL 33458, USA.
Shawn Browning
Jiali Li
Irena Suponitsky-Kroyter
Charles Weissmann
Scripps Institution of Oceanography · USScripps (United States) · USNational Institutes of Health · US

Funding

Emergence of drug resistance in prion populationsR01NS067214 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI SMITH, ROY G · 2010 to 2013
$1.7M
NINDS NIH HHS R01 NS067214PHS HHS NSO59543
6 · The paper itself

Abstract

Prions consist mainly of PrP(Sc), a pathogenic conformer of host-encoded PrP(C). Prion populations with distinct phenotypes but associated with PrP(Sc), having the same amino acid sequence, constitute distinct strains. Strain identity is thought to be encoded by the conformation of PrP(Sc) and to be maintained by seeded conversion. Prion strains can be distinguished by the cell panel assay, which measures their ability to infect distinct cell lines. Brain-derived 22L prions characteristically are able to infect R33 cells (i.e., are "R33 competent"), as well as PK1 cells in the presence of the inhibitor swainsonine (i.e. are "swa resistant"). Here we report that 22L prions retained their characteristic cell tropism and swa resistance when transferred from brain to R33 cells. However, when transferred from the R33 cells to PK1 cells, they gradually became R33 incompetent and swa sensitive, unless the transfer was in the presence of swa, in which case swa resistance and R33 competence were retained. PrP(Sc) associated with swa-resistant/R33-competent and swa-sensitive/R33-incompetent prions had different conformational stabilities. When cloned R33-incompetent/swa-sensitive prions were again propagated in brain, their properties gradually reverted to those of the original brain-derived 22L prions. Our results support the view that 22L prion populations are heterogeneous and that distinct prion variants are selected in different cellular environments.

Indexed as

MutationAnimalsAntineoplastic Agents, PhytogenicBlotting, WesternBrainCell Line, TumorDrug ResistanceGenetic VariationHost SpecificityMiceMice, Inbred C57BLPrionsProtein ConformationPrPSc ProteinsSwainsonineAntineoplastic Agents, PhytogenicPrionsPrPSc ProteinsSwainsonine

Identifiers

PMID21156827
PMCPMC3012531
OpenAlexW2044980031

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.