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Field Postmortem Rabies Rapid Immunochromatographic Diagnostic Test for Resource-Limited Settings with Further Molecular Applications
Published on: June 29, 2020
From rabies to transmissible spongiform encephalopathies: an immune-mediated microbial trigger involving molecular
Alan Ebringer1, Taha Rashid, Noor Jawad
1School of Biomedical and Health Sciences, King's College London, 150 Stamford Street, London SE1 9NN, UK. alan.ebringer@kcl.ac.uk
Abstract:
The concept of experimental allergic encephalomyelitis (EAE) being linked to both rabies post-vaccination encephalomyelitis and multiple sclerosis (MS) has raised the intriguing question whether animal studies carried out for the induction and transmission of transmissible spongiform encephalopathies (TSEs) using brain antigens including prions do have a similar immunopathogenetic mechanism. Although an essential link between autoimmunity and MS has been well established, its role in the pathogenesis of TSEs is generally lacking. However, auto-antibodies to myelin proteins and/or other neuronal antigens such as neurofilaments and prion proteins have been reported in animals with bovine spongiform encephalopathy (BSE) and scrapie as well as in patients with Creutzfeld-Jakob disease (CJD) and kuru. Acinetobacter has been suggested as a possible triggering microbial factor in the initiation of the autoimmune responses in these diseases because bacterial molecular sequences resemble brain antigens, especially in animals affected with BSE and patients with MS and CJD. These possibilities need to be evaluated further with longitudinal prospective studies carried out on larger numbers of animals or humans with such diseases. The transplantation of saline suspensions of brain homogenates will evoke immunological responses and therefore, the results in the study of MS and other neurological diseases have to be interpreted with caution.
Insights
Investigating transmissible spongiform encephalopathies (TSEs), this study explores potential autoimmune mechanisms similar to multiple sclerosis (MS). Autoantibodies and microbial triggers like Acinetobacter are implicated in TSE pathogenesis, warranting further research.
Area of Science:
- Neuroimmunology
- Prion Diseases
- Autoimmunity
Background:
- Experimental allergic encephalomyelitis (EAE) shares links with rabies post-vaccination encephalomyelitis and multiple sclerosis (MS).
- The immunopathogenetic mechanisms of transmissible spongiform encephalopathies (TSEs) remain unclear, particularly regarding autoimmunity.
- Autoantibodies to neuronal antigens (myelin, neurofilaments, prion proteins) have been observed in BSE, scrapie, CJD, and kuru.
Purpose of the Study:
- To investigate potential shared immunopathogenetic mechanisms between TSEs and autoimmune neurological diseases like MS.
- To explore the role of autoantibodies and microbial factors in the pathogenesis of TSEs.
Main Methods:
- Review of existing literature on EAE, MS, TSEs, and associated autoantibodies.
- Consideration of microbial factors, such as Acinetobacter, as potential triggers for autoimmune responses.
Main Results:
- Autoantibodies against brain antigens are reported in animals and humans with TSEs.
- Bacterial molecular sequences resembling brain antigens (e.g., Acinetobacter) are proposed as potential initiators of autoimmune responses in BSE and CJD.
Conclusions:
- Autoimmunity may play a role in the pathogenesis of TSEs, similar to MS.
- Further longitudinal studies are needed to confirm the role of autoantibodies and microbial triggers in TSEs.
- Caution is advised when interpreting studies involving brain homogenates due to potential immunological responses.
Related Concept Videos
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Encephalitis ll: Pathophysiology
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Arboviral Encephalitis
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Microorganisms in Medicine and Therapeutics

