Abstract

Zika virus (ZIKV) is an emerging arthropod-borne virus (arbovirus) belonging to the family Flaviviridae and genus Flavivirus. ZIKV was first isolated from a monkey in the Zika forest of Uganda in 1947 [1]. Subsequently, sporadic human infections were reported in Africa and Asia. In 2007, the first large documented ZIKV outbreak was reported from Yap State, Federated States of Micronesia [2]. No further transmission was identified in the Pacific until October 2013, when French Polynesia (FP) reported the first cases; a subsequent explosive outbreak resulted in an estimated 28 000 cases seeking medical care (approximately 11% of the population) [3,4]. Phylogenetic analyses demonstrated that the FP strain was closely related to Cambodia 2010 and Yap State 2007 strains, corroborating previous findings of the expansion of the ZIKV Asian lineage [3]. During the FP outbreak, most clinical cases presented with mild disease characterized by low-grade fever, maculopapular rash, arthralgia, and conjunctivitis. In November, a patient presented with Guillain–Barre syndrome (GBS), an autoimmune disease causing acute or subacute flaccid paralysis, 1 week after a confirmed acute ZIKV infection [5]. Subsequent GBS cases were identified, correlating temporally with the ZIKV outbreak. The incidence rate of GBS cases during the ZIKV outbreak was approximately 20-fold higher than expected given the size of the FP population and the established incidence rates of GBS (1–2/ 100 000 population per year) [6]. No severe disease resulting from ZIKV infection had been reported prior to the FP outbreak, but previous clinical characterization was based on a limited number of confirmed cases. The recent temporal and spatial association between the FP ZIKV outbreak and the highly unusual GBS cluster is very

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