Abstract
The recent Zika virus (ZIKV) outbreak in the Americas surprised all of us because of its rapid spread and association with neurologic disorders including fetal microcephaly, brain and ocular anomalies, and Guillain–Barré syndrome. In response to this global health crisis, unprecedented and world-wide efforts are taking place to study the ZIKV-related human diseases. Much has been learned about this virus in the areas of epidemiology, genetic diversity, protein structures, and clinical manifestations, such as consequences of ZIKV infection on fetal brain development. However, progress on understanding the molecular mechanism underlying ZIKV-associated neurologic disorders remains elusive. To date, we still lack a good understanding of; (1) what virologic factors are involved in the ZIKV-associated human diseases; (2) which ZIKV protein(s) contributes to the enhanced viral pathogenicity; and (3) how do the newly adapted and pandemic ZIKV strains alter their interactions with the host cells leading to neurologic defects? The goal of this review is to explore the molecular insights into the ZIKV–host interactions with an emphasis on host cell receptor usage for viral entry, cell innate immunity to ZIKV, and the ability of ZIKV to subvert antiviral responses and to cause cytopathic effects. We hope this literature review will inspire additional molecular studies focusing on ZIKV–host Interactions.
Highlights
We have learned a great deal about its epidemiology, genetic diversity, viral pathogenicity, and clinical manifestations that are linked to Zika virus (ZIKV)-associated human neurological diseases
We describe molecular interactions of ZIKV with its host cells
We briefly outline different cell types and receptors utilized by ZIKV for viral entry and infection
Summary
The 2015 Zika virus (ZIKV) epidemic in the Americas surprised the world because of its rapid global spread and the findings that it associates with various neurologic disorders including microcephaly in newborns and Guillain–Barré syndrome (GBS) in adults. ZIKV was thought to be a mild virus that had little or no threat to humans Through studies of this new ZIKV pandemic, we have learned that ZIKV is a rather severe human pathogen that can cause significant neuropathology such as fetal microcephaly, GBS, and various other congenital neurologic and ocular disorders [1,2,3,4,5]. It begs the question of what has transformed a benign ZIKV over the past seventy years to generate the contemporary pathogenic ZIKV. The molecular mechanisms underlying these ZIKV–host interactions, and their potential impacts on ZIKV-induced fetal microcephaly or other neurologic disorders are discussed
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