During 2013-2014, French Polynesia experienced an outbreak of Zika virus infection. Serosurveys conducted at the end of the outbreak and 18 months later showed lower than expected disease prevalence rates (49%) and asymptomatic:symptomatic case ratios (1:1) in the general population but significantly different prevalence rates (66%) and asymptomatic:symptomatic ratios (1:2) in schoolchildren.

French Polynesia is a high epidemic/endemic area for arthropod-borne viruses (arboviruses). We recently reported the silent circulation of Ross River virus and absence of active transmission of chikungunya virus (CHIKV) among blood donors sampled before the emergence of Zika virus (ZIKV) and CHIKV in French Polynesia. In this study, the prevalence of the four serotypes of dengue virus (DENV) and the occurrence of circulation of other arboviruses were investigated in blood donors in French Polynesia. Serum samples from 593 blood donors collected between July 2011 and October 2013 were tested by ELISA for the presence of immunoglobulin G antibodies against each of the four DENV serotypes, ZIKV, Japanese encephalitis virus (JEV), and West Nile virus (WNV). It was found that 80.3%, 0.8%, 1.3%, and 1.5% of blood donors were seropositive for at least one DENV serotype, ZIKV, JEV, and WNV, respectively. These results corroborate the expected high transmission of DENV and conversely suggest that no active circulation of ZIKV, JEV, and WNV occurred in French Polynesia before 2011. Information provided by this study may be useful for public health authorities to improve surveillance and implement strategies to prevent the transmission of arboviruses.

BACKGROUND: Zika virus (ZIKV) is an arthropod‐borne virus (arbovirus) transmitted by mosquitoes. The potential for ZIKV transmission through blood transfusion was demonstrated during the ZIKV outbreak that occurred in French Polynesia from October 2013 to April 2014. Pathogen inactivation of blood products is a proactive strategy that provides the potential to reduce transfusion‐transmitted diseases. Inactivation of arboviruses by amotosalen and ultraviolet A (UVA) illumination was previously demonstrated for chikungunya, West Nile, and dengue viruses. We report here the efficiency of this process for ZIKV inactivation of human plasma.STUDY DESIGN AND METHODS: Plasma units were spiked with ZIKV. Viral titers and RNA loads were measured in plasma before and after amotosalen and UVA photochemical treatment.RESULTS: The mean ZIKV titers and RNA loads in plasma before inactivation were respectively 6.57 log TCID₅₀/mL and 10.25 log copies/mL. After inactivation, the mean ZIKV RNA loads was 9.51 log copies/mL, but cell cultures inoculated with inactivated plasma did not result in infected cells and did not produce any replicative virus after one passage, nor detectable viral RNA from the second passage.CONCLUSION: In this study we demonstrate that amotosalen combined with UVA light inactivates ZIKV in fresh‐frozen plasma. This inactivation process is of particular interest to prevent plasma transfusion‐transmitted ZIKV infections in areas such as French Polynesia, where several arboviruses are cocirculating.

Globally, autosomal recessive IFNAR1 deficiency is a rare inborn error of immunity underlying susceptibility to live attenuated vaccine and wild-type viruses. We report seven children from five unrelated kindreds of western Polynesian ancestry who suffered from severe viral diseases. All the patients are homozygous for the same nonsense IFNAR1 variant (p.Glu386*). This allele encodes a truncated protein that is absent from the cell surface and is loss-of-function. The fibroblasts of the patients do not respond to type I IFNs (IFN-α2, IFN-ω, or IFN-β). Remarkably, this IFNAR1 variant has a minor allele frequency >1% in Samoa and is also observed in the Cook, Society, Marquesas, and Austral islands, as well as Fiji, whereas it is extremely rare or absent in the other populations tested, including those of the Pacific region. Inherited IFNAR1 deficiency should be considered in individuals of Polynesian ancestry with severe viral illnesses.

The epidemiology of dengue in the South Pacific has been characterized by transmission of a single dominant serotype for 3–5 years, with subsequent replacement by another serotype. From 2001 to 2008 only DENV-1 was reported in the Pacific. In 2008, DENV-4 emerged and quickly displaced DENV-1 in the Pacific, except in New Caledonia (NC) where DENV-1 and DENV-4 co-circulated in 2008–2009. During 2012–2013, another DENV-1 outbreak occurred in NC, the third DENV-1 outbreak in a decade. Given that dengue is a serotype-specific immunizing infection, the recurrent outbreaks of a single serotype within a 10-year period was unexpected.