Neurology: Clinical Practice Month, October 4, 2018
Maíra Cardoso Aspahan, Sonja Emily Leonhard, Rodrigo Santiago Gomez, Eder da Silva Rocha, Michelle Ramos da Silva Vilela, Pedro Paulo Martins Alvarenga, Paula Eillanny Silva Marinho, Erna Geessien Kroon, Fidel Meira
The ZIKV epidemic in 2015 in Latin America was followed by an increase in microcephaly and Guillain-Barre syndrome cases, and ZIKV has subsequently been linked to other neurologic complications including myelitis, encephalitis, and acute disseminated encephalomyelitis.
This study follows a rare case reported of NMOSD linked to ZIKV infection in Brazil in 2017. How ZIKV can cause or trigger neurologic disease is not yet fully understood and could be due to direct virus neuro-tropism or immune-mediated processes.
Other viral infections, including DENV, varicella-zoster virus, and cyto-megalovirus, have previously been associated with NMOSD. The suggested pathologic mechanisms include molecular mimicry and increased self-antigen presentation due to tissue destruction. In this NMOSD case report, the positive PCR in the CSF and other biological materials at onset suggest a direct viral pathogenicity. However, new severe neurologic symptoms occurred when PCR for ZIKV was already negative, suggesting a postinfectious or parainfectious mechanism. Furthermore, the preceding DENV infection, as some studies indicate, could intensify ZIKV neurologic manifestations due to cross-reactive antibodies.