Foodborne Transmission of Bovine Spongiform Encephalopathy to Non-Human Primates Results in Preclinical Rapid-Onset Obesity

Strom, Alexander; Yutzy, Barbara; Kruip, Carina; Ooms, Mark; Schloot, Nanette C.; Roden, Michael; Scott, Fraser W.; Loewer, Johannes; Holznagel, Edgar

doi:10.1371/journal.pone.0104343

Cited by 8 publications

(6 citation statements)

References 42 publications

(53 reference statements)

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“…PrP Sc deposits in ganglia of the myenteric plexus were also detectable. Interestingly, animals which received multiple oral doses did not succumb to clinical disease, although PrP had been deposited in the GALT (Strom et al, 2014). This is in keeping with the observation of PrP in the lymphoreticular tissues of vCJD patients (Ironside, 2012), and may indicate a possible explanation for the high prevalence of human appendix samples with PrP accumulation (Gill et al, 2013).…”

Section: In Vivo Methods Using Primates For the Study Of The Moleculasupporting

confidence: 73%

Untitled

2015

EFSA Journal

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The factors that modulate the transmissibility of Transmissible Spongiform Encephalopathies (TSE) and the approaches for the study of their zoonotic potential are reviewed. The paper 'Evidence for zoonotic potential of ovine scrapie prions' by Cassard et al. (2014) is scientifically appraised, focussing on the experimental design, the results and the conclusions. The paper provides evidence in a laboratory experiment that some Classical scrapie isolates can propagate in humanised transgenic mice and produce prions that on second passage are similar to those causing one form of sporadic Creutzfeldt-Jakob disease (sCJD). It is concluded that the results from the study raise the possibility that scrapie prions have the potential to be zoonotic, but do not provide evidence that transmission can or does take place under field conditions. The conclusions of the 2011 ECDC-EFSA 'Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans' are reviewed in the light of the new scientific evidence available since its publication. This supports and strengthens the conclusions of that opinion with regard to the potential for some animal TSE to be zoonotic, but does not provide evidence of a causal link between Classical or Atypical scrapie and human TSE. Current evidence does not establish this link, and no consistent risk factors have been identified for sCJD. The possibility of scrapie-related public health risks from the consumption of ovine products cannot be assessed. Recommendations are formulated on further studies and data that are needed to investigate the zoonotic potential of animal TSE and to estimate the amount of infectivity from TSE-infected products sourced from small ruminants and entering the food chain in the European Union.

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Section: In Vivo Methods Using Primates For the Study Of The Moleculasupporting

confidence: 73%

Untitled

2015

EFSA Journal

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“…Spontaneous diabetes is described in the CM, but it classically occurs in 1-2% of captive monkeys (Clarkson et al, 1985), often in obese animals that represent less than 20% of the general population (Bauer et al, 2010). A correlation between the onset of obesity and diabetes and the infection with prions (BSE in their case) has been described by other authors (Strom et al, 2014). The animals included in the Canadian study were tested for the presence of specific hallmarks of prion disease.…”

Section: Non-human Primate Modelsmentioning

confidence: 80%

Update on chronic wasting disease (CWD) III

Koutsoumanis¹,

Allende²,

Álvarez‐Ordóñez³

et al. 2019

EFS2

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The European Commission asked EFSA for a Scientific Opinion: to revise the state of knowledge about the differences between the chronic wasting disease (CWD) strains found in North America (NA) and Europe and within Europe; to review new scientific evidence on the zoonotic potential of CWD and to provide recommendations to address the potential risks and to identify risk factors for the spread of CWD in the European Union. Full characterisation of European isolates is being pursued, whereas most NA CWD isolates have not been characterised in this way. The differing surveillance programmes in these continents result in biases in the types of cases that can be detected. Preliminary data support the contention that the CWD strains identified in Europe and NA are different and suggest the presence of strain diversity in European cervids. Current data do not allow any conclusion on the implications of strain diversity on transmissibility, pathogenesis or prevalence. Available data do not allow any conclusion on the zoonotic potential of NA or European CWD isolates. The risk of CWD to humans through consumption of meat cannot be directly assessed. At individual level, consumers of meat, meat products and offal derived from CWD-infected cervids will be exposed to the CWD agent(s). Measures to reduce human dietary exposure could be applied, but exclusion from the food chain of whole carcasses of infected animals would be required to eliminate exposure. Based on NA experiences, all the risk factors identified for the spread of CWD may be associated with animals accumulating infectivity in both the peripheral tissues and the central nervous system. A subset of risk factors is relevant for infected animals without involvement of peripheral tissues. All the risk factors should be taken into account due to the potential co-localisation of animals presenting with different disease phenotypes. SummaryIn 2018, the European Food Safety Authority (EFSA) was asked by the European Commission to deliver a Scientific Opinion on three Terms of Reference (ToRs) related to chronic wasting disease (CWD): (ToR1) to revise the state of knowledge, considering new scientific data, about the differences: a) between the strains found in different species in North America (NA) and in Europe and b) between the strains found so far in moose, reindeer and red deer in Europe, with the main emphasis on transmissibility (transmission paths), pathogenicity and prevalence of the different strains and susceptibility of the different species/genotypes; (ToR2) to revise the new scientific evidence on the zoonotic potential of CWD, to assess the risk of transmission to humans through the consumption of fresh meat, meat products and offal of cervids and to provide recommendations on possible additional control measures to address the risks identified; and (ToR3) to identify risk factors that can facilitate the spread of CWD in the European Union given the current situation of the disease.To source the relevant data, the extensive literature searches used in ...

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“…The prion-related Creutzfeldt-Jacob disease in humans leads to bovine spongiform encephalopathy in cattle and macaques. Oral infection of macaques with prions was also shown to cause subsequent rapid weight gain within 1.5 years post infection (Strom et al 2014). In that study, prion accumulation was confined to the gastrointestinal tract and was associated with a change in the density of intestinal glucagon-like peptide-1 (GLP-1) cells.…”

Section: Infection As a Cause Of Obesity Infection-induced Obesity Inmentioning

confidence: 95%

Obesity and Infection: Reciprocal Causality

Hainer

Zamrazilová²,

Kunešová³

et al. 2015

Physiol Res

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Associations between different infectious agents and obesity have been reported in humans for over thirty years. In many cases, as in nosocomial infections, this relationship reflects the greater susceptibility of obese individuals to infection due to impaired immunity. In such cases, the infection is not related to obesity as a causal factor but represents a complication of obesity. In contrast, several infections have been suggested as potential causal factors in human obesity. However, evidence of a causal linkage to human obesity has only been provided for adenovirus 36 (Adv36). This virus activates lipogenic and proinflammatory pathways in adipose tissue, improves insulin sensitivity, lipid profile and hepatic steatosis. The E4orf1 gene of Adv36 exerts insulin senzitizing effects, but is devoid of its pro-inflammatory modalities. The development of a vaccine to prevent Adv36-induced obesity or the use of E4orf1 as a ligand for novel antidiabetic drugs could open new horizons in the prophylaxis and treatment of obesity and diabetes. More experimental and clinical studies are needed to elucidate the mutual relations between infection and obesity, identify additional infectious agents causing human obesity, as well as define the conditions that predispose obese individuals to specific infections.

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Foodborne Transmission of Bovine Spongiform Encephalopathy to Non-Human Primates Results in Preclinical Rapid-Onset Obesity

Cited by 8 publications

References 42 publications

Untitled

Untitled

Update on chronic wasting disease (CWD) III

Obesity and Infection: Reciprocal Causality

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