↓ Skip to main content

Absence of Evidence for a Causal Link between Bovine Spongiform Encephalopathy Strain Variant L-BSE and Known Forms of Sporadic Creutzfeldt-Jakob Disease in Human PrP Transgenic Mice

Overview of attention for article published in Journal of Virology, November 2016
Altmetric Badge

Mentioned by

twitter
2 X users

Citations

dimensions_citation
26 Dimensions

Readers on

mendeley
28 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Absence of Evidence for a Causal Link between Bovine Spongiform Encephalopathy Strain Variant L-BSE and Known Forms of Sporadic Creutzfeldt-Jakob Disease in Human PrP Transgenic Mice
Published in
Journal of Virology, November 2016
DOI 10.1128/jvi.01383-16
Pubmed ID
Authors

Emilie Jaumain, Isabelle Quadrio, Laetitia Herzog, Fabienne Reine, Human Rezaei, Olivier Andréoletti, Hubert Laude, Armand Perret-Liaudet, Stéphane Haïk, Vincent Béringue

Abstract

Prions are proteinaceous pathogens responsible for subacute spongiform encephalopathies in animals and humans. The prions responsible for bovine spongiform encephalopathy (BSE) are zoonotic agents, causing variant Creutzfeldt-Jakob disease (CJD) in humans. The transfer of prions between species is limited by a species barrier, which is thought to reflect structural incompatibilities between host cellular prion protein (PrP(C)) and the infecting pathological PrP assemblies (PrP(Sc)) constituting the prion. A BSE strain variant, designated L-BSE and responsible for atypical, supposedly spontaneous forms of prion diseases in aged cattle, demonstrates zoonotic potential, as evidenced by its capacity to propagate more easily than classical BSE in transgenic mice expressing human PrP(C) and in non-human primates. In humanized mice, L-BSE propagates without any apparent species barrier and shares similar biochemical PrP(Sc) signatures with the CJD subtype designated MM2-cortical, thus opening the possibility that certain CJD cases classified as sporadic may actually originate from L-type BSE cross-transmission. To address this issue, we compared the biological properties of L-BSE and those of a panel of CJD subtypes representative of the human prion strain diversity using standard strain-typing criteria in human PrP transgenic mice. We found no evidence that L-BSE causes a known form of sporadic CJD. Since the quasi-extinction of classical BSE, atypical BSE forms are the sole BSE variants circulating in cattle worldwide. They are observed in rare cases of old cattle, making them difficult to detect. Extrapolation of our results suggests that L-BSE may propagate in humans as an unrecognized form of CJD and we urge both the continued utilization of precautionary measures to eliminate these agents from the human food chain and active surveillance for CJD phenotypes in the general population.

X Demographics

X Demographics

The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 4%
Unknown 27 96%

Demographic breakdown

Readers by professional status Count As %
Researcher 6 21%
Student > Bachelor 5 18%
Student > Master 4 14%
Unspecified 3 11%
Student > Ph. D. Student 2 7%
Other 4 14%
Unknown 4 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 5 18%
Medicine and Dentistry 3 11%
Unspecified 3 11%
Biochemistry, Genetics and Molecular Biology 3 11%
Neuroscience 3 11%
Other 6 21%
Unknown 5 18%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 May 2017.
All research outputs
#17,289,387
of 25,377,790 outputs
Outputs from Journal of Virology
#22,056
of 25,691 outputs
Outputs of similar age
#203,124
of 313,259 outputs
Outputs of similar age from Journal of Virology
#109
of 144 outputs
Altmetric has tracked 25,377,790 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 25,691 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.5. This one is in the 9th percentile – i.e., 9% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 313,259 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 144 others from the same source and published within six weeks on either side of this one. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.