Advances in Zika Virus⁻Host Cell Interaction: Current Knowledge and Future Perspectives.

Jae Lee,Ok Shin

doi:10.3390/ijms20051101

Abstract

Emerging mosquito-transmitted RNA viruses, such as Zika virus (ZIKV) and Chikungunya represent human pathogens of an immense global health problem. In particular, ZIKV has emerged explosively since 2007 to cause a series of epidemics in the South Pacific and most recently in the Americas. Although typical ZIKV infections are asymptomatic, ZIKV infection during pregnancy is increasingly associated with microcephaly and other fetal developmental abnormalities. In the last few years, genomic and molecular investigations have established a remarkable progress on the pathogenic mechanisms of ZIKV infection using in vitro and in vivo models. Here, we highlight recent advances in ZIKV-host cell interaction studies, including cellular targets of ZIKV, ZIKV-mediated cell death mechanisms, host cell restriction factors that limit ZIKV replication, and immune evasion mechanisms utilized by ZIKV. Understanding of the mechanisms of ZIKV–host interaction at the cellular level will contribute crucial insights into the development of ZIKV therapeutics and vaccines.

Highlights

Infectious diseases have gained importance as a significant threat to public health following the recent outbreaks of arthropod-transmitted viruses in the western hemisphere
Of the numerous human pathogens that have experienced a rapid geographic distribution, this review focuses on Zika virus (ZIKV), which has raised international health concerns due to its broad spectrum of transmission routes, autoimmune disorders in adults, and neurodevelopmental complications in newborns [2,3]
ZIKV belongs to the Flaviviridae family along with Japanese encephalitis virus (JEV), West Nile virus (WNV), and dengue virus (DENV), all of which are medically important viruses transmitted by mosquitoes or ticks

Summary

Introduction

Infectious diseases have gained importance as a significant threat to public health following the recent outbreaks of arthropod-transmitted viruses (arboviruses) in the western hemisphere. Diagnosis of ZIKV infection has depended on molecular and serological testing, employing ELISA and RT-PCR platforms for IgM and RNA detection [7]. These methods of diagnosis are only useful for virus detection within a short frame from the symptom onset as levels of viral RNA and IgM antibodies decline over time. Many of these crucial interactions, remain elusive In this Review, we focus on ZIKV, a member of the Flaviviridae family, and highlight the viral pathogenesis at the level of cellular mechanisms and interactions

Structure of ZIKV

Multiple Cell Death Pathways Induced by ZIKV Infection

Host Cell Restriction Factors that Limit ZIKV Replication

Immune Evasion Mechanisms Utilized by ZIKV

Future Directions for ZIKV Studies