Abstract
Mosquito-borne viruses of the Flavivirus genus (Flaviviridae family) pose an ongoing threat to global public health. For example, dengue, Japanese encephalitis, West Nile, yellow fever, and Zika viruses are transmitted by infected mosquitoes and cause severe and fatal diseases in humans. The means by which mosquito-borne flaviviruses establish persistent infection in mosquitoes and cause disease in humans are complex and depend upon a myriad of virus-host interactions, such as those of the innate immune system, which are the main focus of our review. This review also covers the different strategies utilized by mosquito-borne flaviviruses to antagonize the innate immune response in humans and mosquitoes. Given the lack of antiviral therapeutics for mosquito-borne flaviviruses, improving our understanding of these virus-immune interactions could lead to new antiviral therapies and strategies for developing refractory vectors incapable of transmitting these viruses, and can also provide insights into determinants of viral tropism that influence virus emergence into new species.
Highlights
Arthropod-borne viruses of the Flavivirus genus are principally transmitted by mosquitoes and ticks, with some flaviviruses having no known vector or being insect-specific viruses with no vertebrate host [1]
Mosquito-borne flaviviruses of major human public health importance, which are the focus of this review, include dengue virus (DENV), Japanese encephalitis virus (JEV), West Nile virus (WNV), yellow fever virus (YFV), and Zika virus (ZIKV)
Virus-encoded antagonists of mosquito-borne flaviviruses (DENV in purple, ZIKV in green, WNV in light blue, JEV in orange, YFV in black) are able to block these pathways in humans and mosquitoes
Summary
Arthropod-borne viruses (arboviruses) of the Flavivirus genus (family Flaviviridae) are principally transmitted by mosquitoes and ticks, with some flaviviruses having no known vector or being insect-specific viruses with no vertebrate host [1]. Following the detection of mosquito-borne flaviviruses in human cells, the innate immune signaling response is activated, leading eventually to the expression of proinflammatory cytokines and type I IFN (Figure 1). The once double-stranded are sensed by RIG-I and MDA5, which, in turn, allows14-3-3ε these receptors to bind the cytosolic sensor cGAS is able to detect mosquito-borne flaviviruses as they disrupt mitochondrial morphodynamics, leadmitochondrial antiviral signaling (MAVS) protein through 14-3-3ε [26]. Main text for Mosquito-borne flaviviruses block the activation of different signaling molecules including those of TLR signaling in humans (Figure 1). RIG-I and MDA5 for 14-3-3 binding [50] This NS3 motif is partially conserved across several mosquito-borne flaviviruses, including DENV, WNV, and ZIKV; YFV and JEV lack this motif [49]. Homology between the N-terminus of STING and a number of flavivirus NS4Bs [70]
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