Evidence map›Paper›PMID 28355274›Full record

ArticlePLoS pathogens2017

PrPSc formation and clearance as determinants of prion tropism.

Ronald A Shikiya, Katie A Langenfeld, Thomas E Eckland, Jonathan Trinh, Sara A M Holec, Candace K Mathiason, Anthony E Kincaid, Jason C Bartz

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Ronald A ShikiyaDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.ORCID 0000-0002-3607-0276
Katie A LangenfeldDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.
Thomas E EcklandDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.
Jonathan TrinhDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.ORCID 0000-0002-2063-8672
Sara A M HolecDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.ORCID 0000-0003-0800-1115
Candace K MathiasonDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, United States of America.ORCID 0000-0002-5920-4556
Anthony E KincaidDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.
Jason C BartzDepartment of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska, United States of America.ORCID 0000-0003-4081-7886
CHI Health Creighton University Medical Center - Bergan Mercy · USColorado State University · USCreighton University · US

Funding

Detection and Characterization of Blood-borne PrionsR01AI112956 · NIAID · COLORADO STATE UNIVERSITY · PI MATHIASON, CANDACE K. · 2014 to 2024
$4.6M
Nebraska Center for VirologyP30GM103509 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 2012 to 2014
$3.3M
Mechanisms of prion strain selectionR01NS052609 · NINDS · CREIGHTON UNIVERSITY · PI BARTZ, JASON C · 2006 to 2015
$3.2M
CONSTRUCTION OF RESEARCH FACILITYC06RR017417 · NCRR · CREIGHTON UNIVERSITY · PI WILSON, M. ROY · 2002 to 2002
$2.0M
NCRR NIH HHS C06 RR017417NIAID NIH HHS R01 AI112956NIGMS NIH HHS P30 GM103509NINDS NIH HHS R01 NS052609
6 · The paper itself

Abstract

Prion strains are characterized by strain-specific differences in neuropathology but can also differ in incubation period, clinical disease, host-range and tissue tropism. The hyper (HY) and drowsy (DY) strains of hamster-adapted transmissible mink encephalopathy (TME) differ in tissue tropism and susceptibility to infection by extraneural routes of infection. Notably, DY TME is not detected in the secondary lymphoreticular system (LRS) tissues of infected hosts regardless of the route of inoculation. We found that similar to the lymphotropic strain HY TME, DY TME crosses mucosal epithelia, enters draining lymphatic vessels in underlying laminae propriae, and is transported to LRS tissues. Since DY TME causes disease once it enters the peripheral nervous system, the restriction in DY TME pathogenesis is due to its inability to establish infection in LRS tissues, not a failure of transport. To determine if LRS tissues can support DY TME formation, we performed protein misfolding cyclic amplification using DY PrPSc as the seed and spleen homogenate as the source of PrPC. We found that the spleen environment can support DY PrPSc formation, although at lower rates compared to lymphotropic strains, suggesting that the failure of DY TME to establish infection in the spleen is not due to the absence of a strain-specific conversion cofactor. Finally, we provide evidence that DY PrPSc is more susceptible to degradation when compared to PrPSc from other lymphotrophic strains. We hypothesize that the relative rates of PrPSc formation and clearance can influence prion tropism.

Indexed as

PrPSc ProteinsAnimalsBlotting, WesternCricetinaeDisease Models, AnimalImmunohistochemistryMaleMesocricetusPrion DiseasesPrionsPrionsPrPSc Proteins

Identifiers

PMID28355274
PMCPMC5386299
OpenAlexW2599306052

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.