Different viral genes modulate virulence in model mammal hosts and Culex pipiens vector competence in Mediterranean basin lineage 1 West Nile virus strains

West Nile virus (WNV) is a single-stranded positive-sense RNA virus (+ssRNA) belonging to the genus Orthoflavivirus. Its enzootic cycle involves mosquito vectors, mainly Culex, and wild birds as reservoir hosts, while mammals, such as humans and equids, are incidental dead-end hosts. It was first discovered in 1934 in Uganda, and since 1999 has been responsible for frequent outbreaks in humans, horses and wild birds, mostly in America and in Europe. Virus spread, as well as outbreak severity, can be influenced by many ecological factors, such as reservoir host availability, biodiversity, movements and competence, mosquito abundance, distribution and vector competence, by environmental factors such as temperature, land use and precipitation, as well as by virus genetic factors influencing virulence or transmission. Former studies have investigated WNV factors of virulence, but few have compared viral genetic determinants of pathogenicity in different host species, and even fewer have considered the genetic drivers of virus invasiveness and excretion in Culex vector. In this study, we characterized WNV genetic factors implicated in the difference in virulence observed in two lineage 1 WNV strains from the Mediterranean Basin, the first isolated during a significant outbreak reported in Israel in 1998, and the second from a milder outbreak in Italy in 2008. We used an innovative and powerful reverse genetic tool, e.g., ISA (infectious subgenomic amplicons) to generate chimeras between Israel 1998 and Italy 2008 strains, focusing on non-structural (NS) proteins and the 3′UTR non-coding region. We analyzed the replication of these chimeras and their progenitors in mammals, in BALB/cByJ mice, and vector competence in Culex (Cx.) pipiens mosquitoes. Results obtained in BALB/cByJ mice suggest a role of the NS2B/NS3/NS4B/NS5 genomic region in viral attenuation in mammals, while NS4B/NS5/3′UTR regions are important in Cx. pipiens infection and possibly in vector competence

Sustained Low-Level Transmission of Zika and Chikungunya Viruses after Emergence in the Fiji Islands.

Zika and chikungunya viruses were first detected in Fiji in 2015. Examining surveillance and phylogenetic and serologic data, we found evidence of low-level transmission of Zika and chikungunya viruses during 2013-2017, in contrast to the major outbreaks caused by closely related virus strains in other Pacific Island countries

Sustained Low-Level Transmission of Zika and Chikungunya Viruses after Emergence in the Fiji Islands

Zika and chikungunya viruses were first detected in Fiji in 2015. Examining surveillance and phylogenetic and serologic data, we found evidence of low-level transmission of Zika and chikungunya viruses during 2013-2017, in contrast to the major outbreaks caused by closely related virus strains in other Pacific Island countries.This work was part of ISID-Pacific and R-ZERO Pacific programs funded by the French Ministry for Europe and Foreign Affairs (Pacific Fund nos. 06314-09/04/14, 12115-02/09/15, 03016-20/05/16, and 04917-19/07/17). The study also received support from the Embassy of France in the Republic of the Fiji Islands. The study was supported by the French Government’s “Investissement d’Avenir” Program (Labex IBEID no. ANR10-LABX-62-IBEID). C.L.L. was supported by an Australia National Health and Medical Research Council Fellowship (grant no. 1109035). A.J.K. was supported by a Wellcome Trust/Royal Society Sir Henry Dale Fellowship (grant no. 206250/Z/17/Z). The seroprevalence study was part of MSc research work by M.K. performed at the University of the South Pacific

Low chikungunya virus seroprevalence two years after emergence in Fiji

Objectives: In Fiji, autochthonous chikungunya virus (CHIKV) infection was first detected in March 2015. In a previous serosurvey conducted during October–November 2015, we reported a prevalence of anti-CHIKV IgG antibodies of 0.9%. In the present study, we investigated the seroprevalence of CHIKV two years after its emergence in Fiji. Methods: Sera from 320 residents of Fiji recruited in June 2017, from the same cohort of individuals that participated in the serosurvey in 2015, were tested for the presence of IgG antibodies against CHIKV using a recombinant antigen-based microsphere immunoassay. Results: Between 2015 and 2017, CHIKV seroprevalence among residents increased from 0.9% (3/333) to 12.8% (41/320). Of the participants with available serum samples collected in both 2015 and 2017 (n = 200), 31 (15.5%) who were seronegative in 2015 had seroconverted to CHIKV in 2017. Conclusions: Our findings suggest that low-level transmission of CHIKV occurred during the two years followingtheemergenceofthe virus in Fiji.NoCHIKVinfection has been reportedin Fiji since2017, butdue to the presumed low herd immunity of the population, the risk of CHIKV re-emergence is high. Consequently, chikungunya should be considered in the differential diagnosis of acute febrile diseases in Fiji

Zika seroprevalence declines and neutralizing antibodies wane in adults following outbreaks in French Polynesia and Fiji

It has been commonly assumed that Zika virus (ZIKV) infection confers long-term protection against reinfection, preventing ZIKV from re-emerging in previously affected areas for several years. However, the long-term immune response to ZIKV following an outbreak remains poorly documented. We compared results from eight serological surveys before and after known ZIKV outbreaks in French Polynesia and Fiji, including cross-sectional and longitudinal studies. We found evidence of a decline in seroprevalence in both countries over a two-year period following first reported ZIKV transmission. This decline was concentrated in adults, while high seroprevalence persisted in children. In the Fiji cohort, there was also a significant decline in neutralizing antibody titres against ZIKV, but not against dengue viruses that circulated during the same period

Ross River Virus Antibody Prevalence, Fiji Islands, 2013–2015

A unique outbreak of Ross River virus (RRV) infection was reported in Fiji in 1979. In 2013, RRV seroprevalence among residents was 46.5% (362/778). Of the residents who were seronegative in 2013 and retested in 2015, 10.9% (21/192) had seroconverted to RRV, suggesting ongoing endemic circulation of RRV in Fiji

Seroprevalence of Dengue and Chikungunya Virus Antibodies, French Polynesia, 2014–2015

We investigated dengue and chikungunya virus antibody seroprevalence in French Polynesia during 2014–2015. Dengue virus seroprevalence was ≈60% among schoolchildren and >83% among the general population; chikungunya virus seroprevalence was <3% before and 76% after Zika virus emergence (2013). Dengue virus herd immunity may affect Zika virus infection and pathogenesis