| Full text | |
| Author(s): |
Morrey, John D.
[1]
;
Oliveira, Alexandre L. R.
[2]
;
Wang, Hong
[1]
;
Zukor, Katherine
[1]
;
de Castro, Mateus Vidigal
[2]
;
Siddharthan, Venkatraman
[1]
Total Authors: 6
|
| Affiliation: | [1] Utah State Univ, Inst Antiviral Res, Dept Anim Dairy & Vet Sci, 5600 Old Main Hill, Logan, UT 84322 - USA
[2] Univ Estadual Campinas, Inst Biol, Campinas, SP - Brazil
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | SCIENTIFIC REPORTS; v. 9, DEC 20 2019. |
| Web of Science Citations: | 0 |
| Abstract | |
Clinical evidence is mounting that Zika virus can contribute to Guillain-Barre syndrome which causes temporary paralysis, yet the mechanism is unknown. We investigated the mechanism of temporary acute flaccid paralysis caused by Zika virus infection in aged interferon alpha beta-receptor knockout mice used for their susceptibility to infection. Twenty-five to thirty-five percent of mice infected subcutaneously with Zika virus developed motor deficits including acute flaccid paralysis that peaked 8-10 days after viral challenge. These mice recovered within a week. Despite Zika virus infection in the spinal cord, motor neurons were not destroyed. We examined ultrastructures of motor neurons and synapses by transmission electron microscopy. The percent coverage of motor neurons by boutons was reduced by 20%; more specifically, flattened-vesicle boutons were reduced by 46%, and were normalized in recovering mice. Using electromyographic procedures employed in people to help diagnose Guillain-Barre syndrome, we determined that nerve conduction velocities between the sciatic notch and the gastrocnemius muscle were unchanged in paralyzed mice. However, F-wave latencies were increased in paralyzed mice, which suggests that neuropathy may exist between the sciatic notch to the nerve rootlets. Reversible synaptic retraction may be a previously unrecognized cofactor along with peripheral neuropathy for the development of Guillain-Barre syndrome during Zika virus outbreaks. (AU) | |
| FAPESP's process: | 14/06892-3 - Use of mesenchymal stem cells in the CNS/PNS interface: repair of proximal lesions |
| Grantee: | Alexandre Leite Rodrigues de Oliveira |
| Support Opportunities: | Research Projects - Thematic Grants |