Abstract
Understanding Zika virus infection dynamics is essential, as its recent emergence revealed possible devastating neuropathologies in humans, thus causing a major threat to public health worldwide. Recent research allowed breakthrough in our understanding of the virus and host pathogenesis; however, little is known on its impact on its main vector, Aedes aegypti. Here we show how Zika virus targets Aedes aegypti’s neurons and induces changes in its behavior. Results are compared to dengue virus, another flavivirus, which triggers a different pattern of behavioral changes. We used microelectrode array technology to record electrical spiking activity of mosquito primary neurons post infections and discovered that only Zika virus causes an increase in spiking activity of the neuronal network. Confocal microscopy also revealed an increase in synapse connections for Zika virus-infected neuronal networks. Interestingly, the results also showed that mosquito responds to infection by overexpressing glutamate regulatory genes while maintaining virus levels. This neuro-excitation, possibly via glutamate, could contribute to the observed behavioral changes in Zika virus-infected Aedes aegypti females. This study reveals the importance of virus-vector interaction in arbovirus neurotropism, in humans and vector. However, it appears that the consequences differ in the two hosts, with neuropathology in human host, while behavioral changes in the mosquito vector that may be advantageous to the virus.
Highlights
Arbovirus infections transmitted by mosquitoes have great impact on global human health[1]
Zika virus neurotropism in mosquito To confirm the presence of ZIKV in the central nervous systems of orally infected A. aegypti, sections from female mosquito heads were tested two weeks post ZIKV infection using pan-flavivirus anti-non-structural protein 1 (NS1) antibody
Virus impact on mosquito neuron spike activity To validate our hypothesis of the ability of flaviviruses to interfere with neuronal communication, electrophysiological activity was recorded at 2, 3 and 7 days post infection using planar Microelectrodes Array (MEA)[26], a method rarely used with invertebrate[27] or with virus infection
Summary
Arbovirus infections transmitted by mosquitoes have great impact on global human health[1]. The most widely spread mosquito-borne viruses dengue, West Nile, Japanese encephalitis, and more recently Zika[3] cause significant morbidity and mortality. Following the recent outbreaks in the Pacific and the Americas in 2014–2015, studies revealed a strong link between ZIKV infection and neuropathology, i.e., Guillain–Barre syndrome in French Polynesia[5] and the Americas[6], congenital syndrome in new born with microcephaly[7] and ocular abnormalities8, 9,] in South America,[7] and recent records of encephalitis[10, 11] and myelitis in adults[12]. Zika virus neurovirulence has been widely studied with different models, in vitro with human pluripotent stem cell (hPSC)-derived neural progenitor cells and organoids[13, 14], or mouse models[15, 16] with different viral strains from Africa, Asia and Brazil[8, 17]. Most flaviviruses replicate alternately between mammalian hosts and insect vectors, with no Gaburro et al Emerging Microbes & Infections (2018)7:68
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