Abstract
Zika virus (ZIKV) is an emerging RNA virus in the widespread Flavivirus genus. Recently, ZIKV has rapidly spread around the world and has been implicated in human disease, including neurological disorders, triggering public and scientific attention. Understanding how ZIKV causes disease is the highest priority, yet little is known about this virus. Here we examine the currently published data from ZIKV studies to provide the latest understanding of ZIKV genome biology and molecular pathogenesis. The ZIKV genome evolved rapidly from the Flavivirus genus and diverged from the members of this genus, even within the dengue virus cluster to which ZIKV belongs. Genome variations and divergences also exist among ZIKV strains/isolates. These genome divergences might account for the uniqueness of Zika disease. ZIKV infection activates not only the antiviral immune response but also the pro-inflammatory responses associated with disease symptoms. Strikingly, ZIKV activates protein complexes that are functionally associated with disease process, such as glial cell activation and proliferation (for example, Toll-like receptors), apoptosis and cell death, and inflammation. The activation of these complexes may critically contribute to Zika disease. The novel insights into ZIKV genome divergence and disease mechanisms summarized in this review will help accelerate the development of anti-ZIKV strategies.Emerging Microbes & Infections (2017) 6, e13; doi:10.1038/emi.2016.141; published online 22 March 2017
Highlights
Zika virus (ZIKV) is a single-stranded positive-sense RNA arbovirus belonging to the Flavivirus genus of the Flaviviridae family, members of which cause widespread morbidity worldwide.[1]
ZIKV has been linked to Guillain–Barré syndrome (GBS), an autoimmune disease that causes paralysis.[4]
In 1952, it was found in humans, and it was linked to Zika disease in 1964.6 little attention was paid to this virus until 2007, when an outbreak of ‘dengue-like illness’ was reported in the Yap State of Micronesia
Summary
Anyou Wang1*, Stephanie Thurmond2,*, Leonel Islas[1,2], Kingyung Hui[2] and Rong Hai[1,2]. The ZIKV genome evolved rapidly from the Flavivirus genus and diverged from the members of this genus, even within the dengue virus cluster to which ZIKV belongs. Genome variations and divergences exist among ZIKV strains/ isolates. These genome divergences might account for the uniqueness of Zika disease. ZIKV activates protein complexes that are functionally associated with disease process, such as glial cell activation and proliferation (for example, Toll-like receptors), apoptosis and cell death, and inflammation. The activation of these complexes may critically contribute to Zika disease. Emerging Microbes & Infections (2017) 6, e13; doi:10.1038/emi.2016.141; published online 22 March 2017
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