Prevalence of Zika virus infection in wild African primates

Cr, Buechler; Al, Bailey; Am, Weiler; Gl, Barry; Aj, Jasinska; Nb, Freimer; Apetrei, Cristian; Je, Phillips-Conroy; Cj, Jolly; Rogers, Jeffrey; Tc, Friedrich; O'Connor, Deborah L

doi:10.1101/077628

Cited by 2 publications

(4 citation statements)

References 7 publications

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“…9b–d ), implicating that infection of the African ZIKV might produce high NS1 antigenemia. ZIKV has two ecologically distinct transmission cycles: a sylvatic cycle (mosquitoes to non-human primates) and a human cycle (mosquitoes to humans) 27 . Knowledge of ZIKV before 2012 was almost exclusively centered on the enzootic sylvatic cycle in Africa 27 , 28 .…”

mentioning

confidence: 99%

“…ZIKV has two ecologically distinct transmission cycles: a sylvatic cycle (mosquitoes to non-human primates) and a human cycle (mosquitoes to humans) 27 . Knowledge of ZIKV before 2012 was almost exclusively centered on the enzootic sylvatic cycle in Africa 27 , 28 . A mosquito survey in Africa showed that ZIKV was detected in mosquitoes collected in multiple surveyed landscapes, except for indoor locations within villages 28 .…”

mentioning

confidence: 99%

“…A mosquito survey in Africa showed that ZIKV was detected in mosquitoes collected in multiple surveyed landscapes, except for indoor locations within villages 28 . Therefore, we hypothesize that the presence of the NS1 188 th valine might bestow the African lineage of ZIKV with a highly efficient enzootic or epizootic transmission cycle 27 , 28 . Other unknown factor(s) might prevent African ZIKV from efficiently establishing a human cycle.…”

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confidence: 99%

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Evolutionary enhancement of Zika virus infectivity in Aedes aegypti mosquitoes

Liu

et al. 2017

Nature

347

337

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SummaryZika virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013-2014) and South America (2015-2016). Phylogenetic studies reveal that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV is responsible for the recent epidemics in the Americas. However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are limited. We have recently shown that nonstructural protein 1 (NS1) facilitates flavivirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes. Here, we report that the antigenemia of NS1 determines ZIKV infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have more robust NS1 antigenemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at the 188th residue in NS1. ZIKV infectivity was enhanced by this residue substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viremic Type I and II interferon receptor-deficient (ifnagr-/-) C57BL/6 (AG6) mouse. Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased antigenemia of the protein. Enhancement of NS1 antigenemia in infected hosts promotes ZIKV infectivity and prevalence in mosquitoes, which potentially facilitates transmission during the recent ZIKV epidemics.

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confidence: 99%

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Evolutionary enhancement of Zika virus infectivity in Aedes aegypti mosquitoes

Liu

et al. 2017

Nature

347

337

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“…In one example, the nonstructural protein 1 (NS1) enhances viral prevalence in mosquitos and the mammalian population [ 54 ]. Analysis of the African lineages revealed a mutation at the 188th residue, from alanine to valine, which conferred secretability of the NS1 protein [ 54 , 56 ], and this may confer highly efficient enzootic and epizootic transmission [ 54 , 57 , 58 ]. Mutations in the nonstructural protein 3 (NS3) region, have been shown to increase viral replication in the mosquito, while decreasing replication in human cells [ 59 ].…”

Section: Viral Evolution Likely Contributed To Pathogenicitymentioning

confidence: 99%

Causes of Phenotypic Variability and Disabilities after Prenatal Viral Infections

Kousa

Hossain

2021

TropicalMed

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Prenatal viral infection can lead to a spectrum of neurodevelopmental disabilities or fetal demise. These can include microencephaly, global developmental delay, intellectual disability, refractory epilepsy, deafness, retinal defects, and cortical-visual impairment. Each of these clinical conditions can occur on a semi-quantitative to continuous spectrum, from mild to severe disease, and often as a collective of phenotypes. Such serious outcomes result from viruses’ overlapping neuropathology and hosts’ common neuronal and gene regulatory response to infections. The etiology of variability in clinical outcomes is not yet clear, but it may be related to viral, host, vector, and/or environmental risk and protective factors that likely interact in multiple ways. In this perspective of the literature, we work toward understanding the causes of phenotypic variability after prenatal viral infections by highlighting key aspects of the viral lifecycle that can affect human disease, with special attention to the 2015 Zika pandemic. Therefore, this work offers important insights into how viral infections and environmental teratogens affect the prenatal brain, toward our ultimate goal of preventing neurodevelopmental disabilities.

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Prevalence of Zika virus infection in wild African primates

Cited by 2 publications

References 7 publications

Evolutionary enhancement of Zika virus infectivity in Aedes aegypti mosquitoes

Evolutionary enhancement of Zika virus infectivity in Aedes aegypti mosquitoes

Causes of Phenotypic Variability and Disabilities after Prenatal Viral Infections

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