Contributions of Genetic Evolution to Zika Virus Emergence.

Su-Jhen Hung,Sheng-Wen Huang

doi:10.3389/fmicb.2021.655065

Abstract

Mosquito-borne Zika virus (ZIKV) was considered an obscure virus causing only mild or self-limited symptoms until the explosive outbreaks in French Polynesia in 2013–2014 and in the Americas in 2015–2016, resulting in more than 700,000 cases of the disease, with occasional miscarriage and severe congenital birth defects, such as intrauterine growth restriction, fetal microcephaly, and other neurodevelopmental malformations. In this review, we summarized the evolution of ZIKV from a mundane virus to an epidemic virus. ZIKV has acquired a panel of amino acid substitutions during evolution when the virus spread from Africa, Asia, Pacific, through to the Americas. Robust occurrence of mutations in the evolution of ZIKV has increased its epidemic potential. Here we discussed the contributions of these evolutionary mutations to the enhancement of viral pathogenicity and host-mosquito transmission. We further explored the potential hypotheses for the increase in ZIKV activity in recent decades. Through this review, we also explored the hypotheses for the occurrence of the recent ZIKV epidemics and highlighted the potential roles of various factors including pathogen-, host-, vector-related, and environmental factors, which may have synergistically contributed to the ZIKV epidemics.

Highlights

Zika virus (ZIKV) belongs to the genus Flavivirus together with other important mosquito-borne human viruses, such as dengue virus (DENV), West Nile virus, Japanese encephalitis virus, and yellow fever virus
Climate change prM-S139N mutant causes a more severe microcephalic phenotype with a thinner cortex, more robust brain cell apoptosis, and more neuronal progenitor cells (NPCs) differentiation disruption in mice non-structural protein 1 (NS1)-A982V mutation enhances ZIKV transmission in a mosquito-mouse-mosquito transmission cycle NS1-A982V mutation of ZIKV enhances the inhibition of interferon-beta production E-V763M mutation increases ZIKV replication, neurovirulence in neonatal mice, and maternal-to-fetal transmission ZIKV with C-T106A, prM-V123A, NS1-A982V, and non-structural protein 5 (NS5)-M3392V mutations has a fitness advantage
Mosquitoes are more susceptible to the African strains than the Asian strains (Weger-Lucarelli et al, 2016; Azar et al, 2017; Roundy et al, 2017). These studies demonstrate that the Asian strains, responsible for the ZIKV outbreaks in the Pacific and the Americas, were less virulent with lower vector competence than the African strains. Due to this evidence that was counterintuitive to the hypothesis for ZIKV emergence and the epidemic trends of ZIKV after 2007, more recent studies have focused on phenotypic comparison of the ancestral (Cambodia 2010) strain and different contemporary Asian strains isolated after 2010 (Liu et al, 2017; Yuan et al, 2017)

Summary

Introduction

Zika virus (ZIKV) belongs to the genus Flavivirus together with other important mosquito-borne human viruses, such as dengue virus (DENV), West Nile virus, Japanese encephalitis virus, and yellow fever virus. Climate change prM-S139N mutant causes a more severe microcephalic phenotype with a thinner cortex, more robust brain cell apoptosis, and more NPC differentiation disruption in mice NS1-A982V mutation enhances ZIKV transmission in a mosquito-mouse-mosquito transmission cycle NS1-A982V mutation of ZIKV enhances the inhibition of interferon-beta production E-V763M mutation increases ZIKV replication, neurovirulence in neonatal mice, and maternal-to-fetal transmission ZIKV with C-T106A, prM-V123A, NS1-A982V, and NS5-M3392V mutations has a fitness advantage Strain evolved to the Asian lineages, contributes to the increase in CZS severity or transmissibility in mosquito vectors.

Results

Conclusion