1. Background
Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) of the family Flaviviridae and genus Flavivirus [1]. ZIKV was first isolated in 1947 in Uganda [2]; sporadic human cases were reported fromthe 1960s in Asia and Africa [3]. The first ZIKV outbreak outside Africa and Asia occurred in 2007 in Yap Island (Federated States of Micronesia, Pacific) [4] and the largest one from October 2013 to March 2014 in French Polynesia (FP), Pacific [5,6]. Clinical presentation of Zika fever is non-specific; the most common symptoms are rash, fever, arthralgia, myalgia, asthenia and conjunctivitis. Patients usually report mild symptoms, asymptomatic infections have also been described [7]. As there is no abrupt clinical onset, dating the beginning of the illness is subjective [8]. Laboratory Zika fever diagnosis is challenging because there is no “gold standard” diagnosistool. The cross reactivity of antibodies between Flaviviruses [9] limits the use of serology, viral culture is not routinely performed and there is no antigenic detection test available. Acute phase diagnosis relies on molecular technologies [5,9]. During the FP outbreak, we used the real time reverse transcription-PCR (ZIKV RT-PCR) protocol described by Lanciotti et al. during investigations of the ZIKV outbreak on Yap Island [9]. The specificity of this protocol for ZIKV amplification has been confirmed against other arboviruses, especially DENV which was co-circulating in FP during the ZIKV outbreak.