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The article discusses the cases of outbreaks of dengue virus (DENV), chikungunya virus (CHIKV), and Zika virus infections in the islands in the Indian Ocean, Pacific Ocean, and the Caribbean in the past 10 years as of May 2016. Also cited are the factors that led to the emergence of such virus like the presence of vectors such as the Aedes aegypti mosquito, and the perinatal transmission of the Zika virus to a neonate.

The article discusses the case of a female patient in French Polynesia who acquired Chikungunya virus (CHICKV) infection from Guadeloupe. Topics discussed include signs and symptoms of the patient, phylogenetic analysis of the CHIKV strain, and reverse transcriptase polymerase chain reaction (RT-PCR) to confirm the virus. Also discussed are the transmission of CHICKV by Aedes species and the role of foreign travel on the spread of diseases.

ZIKA virus (ZIKV) is an emerging pathogen responsible for neurological disorders and congenital microcephaly. However, the molecular basis for ZIKV neurotropism remains poorly understood. Here, we show that Axl is expressed in human microglia and astrocytes in the developing brain and that it mediates ZIKV infection of glial cells. Axl-mediated ZIKV entry requires the Axl ligand Gas6, which bridges ZIKV particles to glial cells. Following binding, ZIKV is internalized through clathrin-mediated endocytosis and traffics to Rab5+ endosomes to establish productive infection. During entry, the ZIKV/Gas6 complex activates Axl kinase activity, which downmodulates interferon signaling and facilitates infection. ZIKV infection of human glial cells is inhibited by MYD1, an engineered Axl decoy receptor, and by the Axl kinase inhibitor R428. Our results highlight the dual role of Axl during ZIKV infection of glial cells: promoting viral entry and modulating innate immune responses. Therefore, inhibiting Axl function may represent a potential target for future antiviral therapies., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)

Before the outbreak that reached the Americas in 2015, Zika virus (ZIKV) circulated in Asia and the Pacific: these past epidemics can be highly informative on the key parameters driving virus transmission, such as the basic reproduction number (R0). We compare two compartmental models with different mosquito representations, using surveillance and seroprevalence data for several ZIKV outbreaks in Pacific islands (Yap, Micronesia 2007, Tahiti and Moorea, French Polynesia 2013-2014, New Caledonia 2014). Models are estimated in a stochastic framework with recent Bayesian techniques. R0 for the Pacific ZIKV epidemics is estimated between 1.5 and 4.1, the smallest islands displaying higher and more variable values. This relatively low range of R0 suggests that intervention strategies developed for other flaviviruses should enable as, if not more effective control of ZIKV. Our study also highlights the importance of seroprevalence data for precise quantitative analysis of pathogen propagation, to design prevention and control strategies., Competing Interests: The authors declare that no competing interests exist.