1. This case-control study of a Zika virus outbreak in French Polynesia showed that an increased incidence of Guillain-Barré syndrome was associated with recent Zika virus infection.
2. History of past dengue virus infection did not significantly differ between cases and control groups as analyzed via retrospective serum immunoassays.
Evidence Rating Level: 3 (Average)
Study Rundown: During an outbreak of Zika virus between October 2013 and April 2014 in French Polynesia, there was also an increase in the incidence of Guillain-Barré syndrome, an autoimmune disease causing acute paralysis. This study sought to assess the role played by Zika virus and dengue virus infections as risk factors for the development of Guillain-Barré syndrome. Patients diagnosed with Guillain-Barré syndrome were matched with controls who presented with non-febrile illness (control group one), as well as patients with acute Zika virus disease but no neurological symptoms (control group two).
Virological investigations were performed to assess for past and current Zika and dengue virus infection in control groups one and two, respectively. 98% of patients diagnosed with Guillain-Barré syndrome demonstrated evidence of past or current Zika virus infection compared to 56% of patients in controls group one. History of dengue virus infection did not significantly differ between patients with Guillain-Barré syndrome and control groups one and two. Though this study provides the first evidence of Zika virus as a potential cause of Guillain-Barré syndrome, it was limited in that retrospective serum samples were unable to be tested for rising antibody titers to absolutely confirm recent Zika virus infection.
In-Depth [case-control study]: This case-control study investigated the role played by Zika virus and dengue virus infection as risk factors for Guillain-Barré syndrome. During a Zika virus outbreak in French Polynesia, patients with Guillain-Barré syndrome (cases) were sex-matched, age-matched, and residence matched to patients with non-febrile illness (control group one; n=98) as well as age-matched to patients with acute Zika virus disease but no neurological symptoms (control group two; n=70). Diagnosis of infection was done through the use of Zika virus-specific RT-PCR, and seroneutralization and microsphere immunofluoroescent assays for both Zika and dengue virus. In patients with Guillain-Barré syndrome, anti-glycolipid reactivity was analyzed via ELISA and combinatorial assays.
Of 42 patients with Guillain-Barré syndrome, 41 (98%) demonstrated anti-Zika IgM or IgG, and all had neutralizing antibodies against Zika virus as opposed to 54 (56%) of 98 in control group one (p<0.0001). Anti-glycolipid activity was demonstrated by ELISA in 13 (31%) patients and by glycoarray in 19 (46%) patients. Past history of dengue virus did not significantly differ between Guillain-Barré syndrome patients and those in control groups one and two (95%, 89%, and 83%, respectively.)
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