Concurrent Guillain-Barré syndrome, transverse myelitis and encephalitis post-Zika: A case report and review of the pathogenic role of multiple arboviral immunity

Abstract

We review post-infectious and post-vaccination neurological syndromes involving peripheral and central nervous system (CNS) and report an illustrative case of simultaneous occurrence of Guillain-Barré syndrome (GBS), confirmed by nerve conduction velocities, plus MRI-demonstrated transverse myelitis (TM) and acute encephalitis [acute disseminated encephalomyelitis] (ADEM+GBS) affecting a 24-year-old woman from Cúcuta, Colombia, who developed acute Zika virus (ZIKV) infection confirmed by serum reverse transcriptase-polymerase chain reaction (RT-PCR) and convalescent ZIKV IgG antibodies. With intensive care treatment, respiratory support, steroids, and intravenous immunoglobulin (IVIg), patient survived with residual flaccid paraparesis. She had preexisting immunity against Chikungunya virus (CHIKV) and Dengue virus (DENV) acquired before the arrival of ZIKV in Colombia. From reports in the Caribbean, Central and South America we review 19 cases of ZIKV-associated TM, encephalitis and ADEM occurring after a mean latent period of 10.5 days (range 1-96) post-infection. Although GBS and ADEM are usually considered post-infectious and associated with development of antibodies against peripheral nerve and CNS epitopes, we postulate that our case of ADEM+GBS is para-infectious, induced by acute ZIKV neurotropism boosted by active immunity against other arboviruses. Animal models of ZIKV demonstrated strong viral neurotropism enhanced by passive immunity with antibodies against arboviruses such as West Nile virus, CHIKV, or DENV. These considerations are relevant to prevent potential ZIKV vaccine-induced reactions involving central and peripheral nervous system.cycle where transmission to humans occurs mainly by female Aedes mosquitoes-also carriers of DENV and Chikungunya (CHIKV), an alphavirus of the family Togaviridae. In addition, sexual transmission of ZIKV has been demonstrated with virus isolations from urine, semen, blood, maternal milk and tears. Zika infection is manifested by fever, maculopapular rash, conjunctivitis and rare uveitis, arthralgias, muscle pain and headache, but about 80% of infections are asymptomatic [2]. Nonetheless, ZIKV is neuroinvasive and capable of causing numerous neurological manifestations [2].According to the World Health Organization (WHO) [3], a major

Molecular Mimicry between Zika virus and central nervous system inflammatory demyelinating disorders: the role of NS5 Zika virus epitope and PLP autoantigens

“…A recent case report identi ed concurrent GBS and ADEM in a 24-year-old woman who developed acute ZikV infection. The authors postulate this case was para-infectious, induced by neurotropism and activation of an immune response against ZikV (23). This same mechanism is probably involved in the development of this NMOSD phenotype in our patient.…”

Guillain-Barré syndrome after SARS-CoV-2 infection in an international prospective cohort study

“…The combination of GBS and myelitis has previously been described in relation to Zika virus. 36 Another patient with myelitis after SARS-CoV-2 infection was initially included in this study, but ultimately excluded because the diagnosis of GBS was subsequently refuted. Other cases of myelitis following SARS-CoV-2 infection have also been published in the past year.…”

Molecular mimicry between Zika virus and central nervous system inflammatory demyelinating disorders: the role of NS5 Zika virus epitope and PLP autoantigens

“…The authors postulate this case was para-infectious, induced by neurotropism and activation of an immune response against ZikV. 24 This same mechanism is probably involved in the development of this NMOSD phenotype in our patient 2.…”

“…The authors postulate this case was para-infectious, induced by neurotropism and activation of an immune response against ZikV. 24 This same mechanism is probably involved in the development of this NMOSD phenotype in our patient 2. Patient 3 could be classified as having a clinical isolated syndrome (CIS) with a high risk of conversion to MS due to the distribution and number of T2 white matter lesions.…”