Variation in<i>Aedes aegypti</i>Mosquito Competence for Zika Virus Transmission

Roundy, Christopher M.; Azar, Sasha R.; Rossi, Shannan L.; Huang, Jing; Leal, Grace; Yun, Ruimei; Fernández‐Salas, Ildefonso; Vitek, Christopher J.; Paploski, Igor Adolfo Dexheimer; Kitron, Uriel; Ribeiro, Guilherme S.; Hanley, Kathryn A.; Weaver, Scott C.; Vasilakis, Nikos

doi:10.3201/eid2304.161484

Cited by 164 publications

(203 citation statements)

References 37 publications

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“…On day 7 post-feeding, engorged mosquitos with similar blood meal sizes were analyzed for the presence of virus in the bodies to estimate viral infection rates. Consistent with previous findings (Roundy et al, 2017), WT virus showed an infection rate of 48% (Fig. 6).…”

Section: Resultssupporting

confidence: 92%

Functional Analysis of Glycosylation of Zika Virus Envelope Protein

et al. 2017

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Summary Zika virus (ZIKV) infection causes devastating congenital abnormities and Guillain-Barré syndrome. The ZIKV envelope (E) protein is responsible for viral entry and represents a major determinant for viral pathogenesis. Like other flaviviruses, the ZIKV E protein is glycosylated at amino acid N154. To study the function of E glycosylation, we generated a recombinant N154Q ZIKV that lacks the E glycosylation, and analyzed the mutant virus in mammalian and mosquito hosts. In mouse models, the mutant was attenuated, as evidenced by lower viremia, decreased weight loss, and no mortality; however, knockout of E glycosylation did not significantly affect neurovirulence. Mice immunized with the mutant virus developed a robust neutralizing antibody response and were completely protected from wild-type ZIKV challenge. In mosquitoes, the mutant virus exhibited diminished oral infectivity for the Aedes aegypti vector. Collectively, the results demonstrate that the E glycosylation is critical for ZIKV infection of mammalian and mosquito hosts.

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Section: Resultssupporting

confidence: 92%

Functional Analysis of Glycosylation of Zika Virus Envelope Protein

et al. 2017

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“…However, recent in vivo and in vitro experimental work using a limited number of ZIKV strains demonstrated that the African lineage exhibits increased fitness/virulence in vertebrates as well as mosquito vectors compared to Asian lineage strains (Bowen et al, 2017; Weger-Lucarelli et al, 2016; Lazear et al, 2016; Roundy et al, 2017; Azar et al, 2017). Characterization of additional African strains in mosquito vectors, reservoir hosts and models for human infection, including early African isolates not available in reference collections are needed to fully explore the evolution of ZIKV, as well as to identify mutations potentially associated with differing phenotypes.…”

Section: Emergence and Spread Of Zikv Infectionmentioning

confidence: 99%

“…ZIKV transmission in the urban cycle mainly involves the anthropophilic Ae. aegypti mosquito (Marchette et al, 1969; Weger-Lucarelli et al, 2016; Roundy et al, 2017; Olson et al, 1981; Guerbois et al, 2016; Li et al, 2012; Boorman and Porterfield, 1956; Cornet et al, 1979b; Hall-Mendelin et al, 2016; Richard et al, 2016; Chouin-Carneiro et al, 2016), and to lesser degree the peridomestic Ae. albopictus (Azar et al, 2017; Grard et al, 2014; Wong et al, 2013), Ae.…”

Section: Mosquito Transmission and Control Measures (Nikos Vasilakis)mentioning

confidence: 99%

“…aegypti mosquitoes, or for higher viremia in humans, which could enhance fetal infection. To date, most experimental studies (Weger-Lucarelli et al, 2016; Roundy et al, 2017; Azar et al, 2017) have failed to support these hypotheses, and cases of microcephaly possibly associated with maternal ZIKV infection in Thailand, Vietnam and Guinea Bissau (Gulland, 2016) suggest that Asian and African ZIKV strains may be capable of producing CZS. However, a recent study reported that NS1 antigen levels affect ZIKV oral infectivity of Ae.…”

Section: Mosquito Transmission and Control Measures (Nikos Vasilakis)mentioning

confidence: 99%

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Zika in the Americas, year 2: What have we learned? What gaps remain? A report from the Global Virus Network

et al. 2017

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In response to the outbreak of Zika virus (ZIKV) infection in the Western Hemisphere and the recognition of a causal association with fetal malformations, the Global Virus Network (GVN) assembled an international taskforce of virologists to promote basic research, recommend public health measures and encourage the rapid development of vaccines, antiviral therapies and new diagnostic tests. In this article, taskforce members and other experts review what has been learned about ZIKV-induced disease in humans, its modes of transmission and the cause and nature of associated congenital manifestations. After describing the make-up of the taskforce, we summarize the emergence of ZIKV in the Americas, Africa and Asia, its spread by mosquitoes, and current control measures. We then review the spectrum of primary ZIKV-induced disease in adults and children, sites of persistent infection and sexual transmission, then examine what has been learned about maternal-fetal transmission and the congenital Zika syndrome, including knowledge obtained from studies in laboratory animals. Subsequent sections focus on vaccine development, antiviral therapeutics and new diagnostic tests. After reviewing current understanding of the mechanisms of emergence of Zika virus, we consider the likely future of the pandemic.

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“…aegypti and Ae. albopictus mosquitoes, which are associated with a risk of local transmission [15] as well other aedine species were heterogeneously and weakly competent for transmission [16][17][18][19][20][21][22][23][24][25]. Therefore, the potential role of other anthropophilic mosquitoes in the ZIKV outbreak raised a question which took time to be addressed [26].…”

mentioning

confidence: 99%

Culex quinquefasciatus mosquitoes do not support replication of Zika virus

Lourenço‐de‐Oliveira

Marques

Sreenu

et al. 2018

Journal of General Virology

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The rapid spread of Zika virus (ZIKV) in the Americas raised many questions about the role of Culex quinquefasciatus mosquitoes in transmission, in addition to the key role played by the vector Aedes aegypti. Here we analysed the competence of Cx. quinquefasciatus (with or without Wolbachia endosymbionts) for a ZIKV isolate. We also examined the induction of RNA interference pathways after viral challenge and the production of small virus-derived RNAs. We did not observe any infection nor such small virus-derived RNAs, regardless of the presence or absence of Wolbachia. Thus, Cx. quinquefasciatus does not support ZIKV replication and Wolbachia is not involved in producing this phenotype. In short, these mosquitoes are very unlikely to play a role in transmission of ZIKV. Micronesia and then in French Polynesia in 2013-2014, and after affecting most of the South Pacific islands, the virus was eventually detected in the Americas in 2015 [1][2][3][4]. The increased number of infections in humans included cases with unusually severe symptoms such as Guillain-Barr e syndrome and developmental abnormalities in newborns that are now described as congenital Zika syndrome [5][6][7][8]. As there are currently no licensed vaccines or specific therapies, the only way to interrupt ZIKV transmission is by controlling mosquito populations [9]. An enzootic cycle limited to Africa and Asia with occasional spillover events has been described [10,11]. In the current outbreak in the Americas, ZIKV is believed to be mainly transmitted by the human-biting mosquito Aedes aegypti [12,13]. Whether a similar enzootic cycle in the Americas can be established is not known and it has been suggested that such a process would make eradication efforts 'practically impossible' [14]. Experimental infections with the epidemic ZIKV genotypes demonstrated that populations of Ae. aegypti and Ae. albopictus mosquitoes, which are associated with a risk of local transmission [15] as well other aedine species were heterogeneously and weakly competent for transmission [16][17][18][19][20][21][22][23][24][25]. Therefore, the potential role of other anthropophilic mosquitoes in the ZIKV outbreak raised a question which took time to be addressed [26]. Culex quinquefasciatus Say is an opportunistic blood feeder predominant in urban settings throughout the tropics where it is frequently the most annoying biting pest to humans [27]. This night-active mosquito is also the vector of many pathogens including arboviruses such as West Nile and St. Louis encephalitis viruses [28], which belong to the genus Flavivirus of the family Flaviviridae and are related to ZIKV. Both Cx. quinquefasciatus and Culex pipiens (from temperate regions) mosquitoes of the Cx. pipiens complex were not able to experimentally transmit ZIKV and no viral particles were detected in mosquito saliva up to 21 days after exposure to an infectious blood meal [17-20, 25, 29-36], though different results were recorded with other Cx. quinquefasciatus strains [37,38]. Even after injection o...

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Variation inAedes aegyptiMosquito Competence for Zika Virus Transmission

Cited by 164 publications

References 37 publications

Functional Analysis of Glycosylation of Zika Virus Envelope Protein

Functional Analysis of Glycosylation of Zika Virus Envelope Protein

Zika in the Americas, year 2: What have we learned? What gaps remain? A report from the Global Virus Network

Culex quinquefasciatus mosquitoes do not support replication of Zika virus

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