Abstract
The Zika virus (ZIKV) is a recently emerged mosquito-borne flavivirus that, while typically asymptomatic, can cause neurological symptoms in adults and birth defects in babies born to infected mothers. The interactions of ZIKV with many different pathways in the human host ultimately determine successful virus replication and ZIKV-induced pathogenesis; however, the molecular mechanisms of such host-ZIKV interactions have just begun to be elucidated. Here, we summarize the recent advances that defined the mechanisms by which ZIKV antagonizes antiviral innate immune signaling pathways, with a particular focus on evasion of the type I interferon response in the human host. Furthermore, we describe emerging evidence that indicated the contribution of several cell-intrinsic mechanisms to an effective restriction of ZIKV infection, such as nonsense-mediated mRNA decay, stress granule formation, and “reticulophagy”, a type of selective autophagy. Finally, we summarize the recent work that identified strategies by which ZIKV modulated these intrinsic antiviral responses.
Highlights
Zika virus (ZIKV) is a member of the Flaviviridae, which is comprised of enveloped viruses with a positive sense, single-stranded RNA genome [1]
This study showed that knockout of PDLIM2 resulted in less efficient IFN-α-mediated STAT2 degradation; STAT2 degradation during flavivirus infection was not investigated in PDLIM2–/– cells [98]
While many viral mechanisms of innate immune antagonism have been elucidated, most studies have focused on those mediated by direct actions of ZIKV NS proteins
Summary
Zika virus (ZIKV) is a member of the Flaviviridae, which is comprised of enveloped viruses with a positive sense, single-stranded RNA genome [1]. The structural proteins C, prM/M, and E, in addition to several NS proteins, are involved in virion assembly at ER membranes and in viral egress from the cell [17]. Besides their central roles in the viral lifecycle, both the NS proteins and sfRNAs of ZIKV (and flaviviruses in general) modulate various innate and intrinsic pathways in the host. A detailed understanding of the mechanisms that ZIKV uses to evade or suppress host intrinsic or innate antiviral pathways might provide novel avenues for the development of antiviral drugs against ZIKV
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