Letter re: Acute Zika infection with concurrent onset of Guillain-BarrÉ syndrome

Siu et al.1 reported the concurrent onset of polyradiculoneuritis and acute Zika virus (ZIKV) infection, while the virus was not cleared from the serum. Guillain-Barré syndrome (GBS) is usually described as a postinfectious disease during which progressive flaccid paralysis develops after a phase of latency following infection. In the most common pathogenetic framework, this free interval permits the generation of sufficient levels of antibodies that cross-react by molecular mimicry with specific components of peripheral nerves, causing myelin or axonal injury, as previously documented with ZIKV infection.2 However, this case report suggested other mechanisms. Given ZIKV cross-reactivity with dengue virus and increasing reports of ZIKV-associated GBS in dengue-seropositive patients,1,3 a hyperacute immune response is possible.4 Given prolonged ZIKV shedding in bodily fluids, and the overlap between GBS onset and persistent shedding in fomites, a direct viral neuropathic effect may also contribute to ZIKV-associated GBS.4 Indeed, ZIKV is able to infect cranial neural crest cells that stem Schwann cell formation.5 ZIKV-associated GBS could reflect a direct viral neuropathic effect on the blood–nerve barrier, allowing cross-reactive antibodies formed during previous infections to have a deleterious effect on nerve function.