Stiftung Tierärztliche Hochschule Hannover (TiHo)

Virus-triggered spinal cord demyelination is followed by a peripheral neuropathy resembling features of Guillain-Barré Syndrome

Affiliation
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany.
Leitzen, Eva;
Affiliation
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany.
Raddatz, Barbara B;
Affiliation
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany.
Jin, Wen;
ORCID
0000-0001-8343-9972
Affiliation
Department of Neurogenetics, Max-Planck-Institute for Experimental Medicine, Hermann-Rein-Straße 3, 37075, Göttingen, Germany.
Goebbels, Sandra;
GND
1133047645
ORCID
0000-0001-8724-9666
Affiliation
Center for Systems Neuroscience, Hannover, Germany.
Nave, Klaus-Armin;
GND
142929565
ORCID
0000-0001-8151-5644
Affiliation
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany. Wolfgang.Baumgaertner@tiho-hannover.de.
Baumgärtner, Wolfgang;
ORCID
0000-0001-6064-7728
Affiliation
Department of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany.
Hansmann, Florian

Theiler's murine encephalomyelitis virus (TMEV)-induces a demyelinating disease in the spinal cord (SC) of susceptible but not in resistant (B6) mouse strains. The aim of the present study was to induce SC demyelination and a peripheral neuropathy in resistant mice by switching the infection site from cerebrum to SC. B6 mice were intraspinally inoculated with TMEV. Infected mice showed clinical signs starting at 7 days post infection (dpi). Histopathology revealed a mononuclear myelitis, centred on the injection site at 3 dpi with subsequent antero- and retrograde spread, accompanied by demyelination and axonal damage within the SC. Virus protein was detected in the SC at all time points. SC inflammation decreased until the end of the investigation period (28 dpi). Concurrent with the amelioration of SC inflammation, the emergence of a peripheral neuropathy, characterized by axonal damage, demyelination and macrophage infiltration, contributing to persistent clinical sings, was observed. Intraspinal TMEV infection of resistant mice induced inflammation, demyelination and delayed viral clearance in the spinal cord and more interestingly, subsequent, virus-triggered inflammation and degeneration within the PN associated with dramatic and progressive clinical signs. The lesions observed in the PN resemble important features of Guillain-Barré syndrome, especially of acute motor/motor-sensory axonal forms.

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