Zika virus genome biology and molecular pathogenesis

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.

Pathogenic viruses: Molecular detection and characterization

“…Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that causes Zika viral disease in human. The recent outbreak of the disease and the wide spread of the virus has caused worldwide fear and triggered scientific effort to study this virus in attempt to accelerate the development of intervention strategies aimed to prevent and treat Zika disease (Wang et al, 2017). The ZIKV genome is single-stranded positive-sense RNA harboring a single open reading frame.…”

“…The virus enters host cells through receptor-mediated endocytosis. The virus entry and replication stimulates the host antiviral and proinflammatory responses, apoptosis, and disrupts regulation of glial cell proliferation (Wang et al, 2017). The N-linked glycosylation of the envelope (E) protein and the precursor membrane (prM) protein (Nambala and Su, 2018) have been indicated to be important determinants of the Zika virus virulence and neuroinvasion (Annamalai et al, 2017).…”

“…Although ZIKV has been known as an arthropod-borne virus with Aedes species mosquitoes as the primary vector, multiple routes of ZIKV transmission have been identified. It has been reported that Zika virus can also be transmitted from human to human through sexual contact, blood transfusion, and vertical transmission from mother to fetus (Gregory et al, 2017;Wang et al, 2017). The Zika virus causes similar symptoms to those caused by Dengue and Chikungunya viruses.…”

The immunopathogenesis of Zika virus: an overview

“…Being together of the mentioned immune factors leads to strong inflammatory response and major tissue damages, that these can confirm this infection can cause GBS [3]. Along with all of the above, regarding the harmful effects of the virus, the human immune system also has some functions.…”

Mitigating the risk of Zika virus contamination of raw materials and cell lines in the manufacture of biologicals

“…ZIKV is an emerging arthropod-borne member of the Flaviviridae virus family and is closely related to other mosquitoborne arboviruses such as dengue virus, yellow fever virus, WNV and Japanese encephalitis virus [6][7][8][9]. The introduction of ZIKV in the Americas in 2015 [10,11] highlighted its epidemic potential and global public health burden [12,13].…”