0 Cao-Lormeau, V. M. Blake, V. M. Mons, S. Lastere, S. Roche, C. Vanhomwegen, J. Dub, T. Baudouin, L. Teissier, A. Larre, P. Vial, A. L. Decam, C. Choumet, V. Halstead, S. K. Willison, H. J. Musset, L. Manuguerra, J. C. Despres, P. Fournie 2016 Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study Lancet 387 1531-9 2016 <p>Background<br />Between October, 2013, and April, 2014, French Polynesia experienced the largest Zika virus outbreak ever described at that time. During the same period, an increase in Guillain-Barr&eacute; syndrome was reported, suggesting a possible association between Zika virus and Guillain-Barr&eacute; syndrome. We aimed to assess the role of Zika virus and dengue virus infection in developing Guillain-Barr&eacute; syndrome.<br />Methods<br />In this case-control study, cases were patients with Guillain-Barr&eacute; syndrome diagnosed at the Centre Hospitalier de Polyn&eacute;sie Fran&ccedil;aise (Papeete, Tahiti, French Polynesia) during the outbreak period. Controls were age-matched, sex-matched, and residence-matched patients who presented at the hospital with a non-febrile illness (control group 1; n=98) and age-matched patients with acute Zika virus disease and no neurological symptoms (control group 2; n=70). Virological investigations included RT-PCR for Zika virus, and both microsphere immunofluorescent and seroneutralisation assays for Zika virus and dengue virus. Anti-glycolipid reactivity was studied in patients with Guillain-Barr&eacute; syndrome using both ELISA and combinatorial microarrays.<br />Findings<br />42 patients were diagnosed with Guillain-Barr&eacute; syndrome during the study period. 41 (98%) patients with Guillain-Barr&eacute; syndrome had anti-Zika virus IgM or IgG, and all (100%) had neutralising antibodies against Zika virus compared with 54 (56%) of 98 in control group 1 (p&lt;0&middot;0001). 39 (93%) patients with Guillain-Barr&eacute; syndrome had Zika virus IgM and 37 (88%) had experienced a transient illness in a median of 6 days (IQR 4&ndash;10) before the onset of neurological symptoms, suggesting recent Zika virus infection. Patients with Guillain-Barr&eacute; syndrome had electrophysiological findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median duration of the installation and plateau phases was 6 [IQR 4&ndash;9] and 4 days [3&ndash;10], respectively). 12 (29%) patients required respiratory assistance. No patients died. Anti-glycolipid antibody activity was found in 13 (31%) patients, and notably against GA1 in eight (19%) patients, by ELISA and 19 (46%) of 41 by glycoarray at admission. The typical AMAN-associated anti-ganglioside antibodies were rarely present. Past dengue virus history did not differ significantly between patients with Guillain-Barr&eacute; syndrome and those in the two control groups (95%, 89%, and 83%, respectively).<br />Interpretation<br />This is the first study providing evidence for Zika virus infection causing Guillain-Barr&eacute; syndrome. Because Zika virus is spreading rapidly across the Americas, at risk countries need to prepare for adequate intensive care beds capacity to manage patients with Guillain-Barr&eacute; syndrome.<br />Funding<br />Labex Integrative Biology of Emerging Infectious Diseases, EU 7th framework program PREDEMICS. and Wellcome Trust.</p>