Abstract
Zika Virus (ZIKV) and Dengue Virus (DENV) are related viruses of the Flavivirus genus that cause significant disease in humans. Existing control measures have been ineffective at curbing the increasing global incidence of infection for both viruses and they are therefore prime targets for new vaccination strategies. Type-I interferon (IFN) responses are important in clearing viral infection and for generating efficient adaptive immune responses towards infection and vaccination. However, ZIKV and DENV have evolved multiple molecular mechanisms to evade type-I IFN production. This review covers the molecular interactions, from detection to evasion, of these viruses with the type-I IFN response. Additionally, we discuss how this knowledge can be exploited to improve the design of new vaccine strategies.
Highlights
Dengue Virus (DENV) and Zika Virus (ZIKV) are closely related viruses of the Flavivirus genus and most infections in humans are asymptomatic, both viruses can cause severe life threatening or debilitating disease
pathogen associated molecular patterns (PAMPs) bind to host germline encoded pattern recognition receptors (PRRs) on the cell surface, within endosomes or in the cytoplasm, leading to recognition leads to activation of complex signaling pathways and the upregulation of multiple innate immune effector molecules and cytokines
Detection of viral RNAs can occur in the endosomal compartment by the membrane associated Toll-like receptors-3 or 7 (TLR) [31]. Both ZIKV and DENV infection results in host mitochondrial DNA release that is sensed by cyclic GMP-AMP synthase and signals through the endoplasmic reticulum (ER) associated intermediate stimulator of interferon genes (STING) [31,33,34]
Summary
Dengue Virus (DENV) and Zika Virus (ZIKV) are closely related viruses of the Flavivirus genus and most infections in humans are asymptomatic, both viruses can cause severe life threatening or debilitating disease. Once produced and secreted by infected cells these antiviral cytokines can act on the same cell or neighboring cells expressing their cognate receptor to initiate signaling that leads to the production of hundreds of interferon stimulated genes (ISGs) [10] These ISGs carry out a range of direct antiviral, regulatory or immunomodulatory functions giving rise to an antiviral state within host cells and tissues [11]. Because of this strong selective pressure many viruses have evolved mechanisms to counteract IFN responses, allowing them to gain a foothold and cause infection Flaviviruses such as ZIKV and DENV have evolved a complex array of molecular interactions with the host innate immune response to undermine both the production and downstream signaling of IFNs. This review aims to summarize the current knowledge of the molecular interactions between. We explain the relevant aspects of Flavivirus virology and lifecycle
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