Abstract
Zika virus (ZIKV) became a public health emergency of global concern in 2015 due to its rapid expansion from French Polynesia to Brazil, spreading quickly throughout the Americas. Its unexpected correlation to neurological impairments and defects, now known as congenital Zika syndrome, brought on an urgency to characterize the pathology and develop safe, effective vaccines. ZIKV genetic analyses have identified two major lineages, Asian and African, which have undergone substantial changes during the past 50 years. Although ZIKV infections have been circulating throughout Africa and Asia for the later part of the 20th century, the symptoms were mild and not associated with serious pathology until now. ZIKV evolution also took the form of novel modes of transmission, including maternal–fetal transmission, sexual transmission, and transmission through the eye. The African and Asian lineages have demonstrated differential pathogenesis and molecular responses in vitro and in vivo. The limited number of human infections prior to the 21st century restricted ZIKV research to in vitro studies, but current animal studies utilize mice deficient in type I interferon (IFN) signaling in order to invoke enhanced viral pathogenesis. This review examines ZIKV strain differences from an evolutionary perspective, discussing how these differentially impact pathogenesis via host immune responses that modulate IFN signaling, and how these differential effects dictate the future of ZIKV vaccine candidates.
Highlights
Zika virus (ZIKV) has garnered international attention due to its rapid worldwide expansion since 2015 when an epidemic struck Brazil, resulting in a newly identified pathology including severe neurological impairments such as microcephaly, which is part of the congenital ZIKV syndrome, as well as Guillain–Barré syndrome (GBS) afflicting adults [1]
This study demonstrates that upon infection of neural tissues with ZIKV, cells from the congenital Zika virus syndrome (CZS) twins grew slower and exhibited increased viral replication
Zika virus hid from the public eye for several decades since it’s discovery in the 1940s, as many cases of ZIKV infections are believed to have either been subclinical or misdiagnosed as a different flavivirus infection, such as dengue virus type 1–4 (DENV)
Summary
Zika virus (ZIKV) has garnered international attention due to its rapid worldwide expansion since 2015 when an epidemic struck Brazil, resulting in a newly identified pathology including severe neurological impairments such as microcephaly, which is part of the congenital ZIKV syndrome, as well as Guillain–Barré syndrome (GBS) afflicting adults [1]. The mounting evidence that ZIKV is causing neuropathology and fetal brain disruption, as well as rising concerns over novel modes of ZIKV transmission suggests an evolutionary change in the molecular and genetic structure of ZIKV strains that has contributed to its rapid expansion, severity of pathogenicity, and multiple routes of infections. These increasing adverse effects depicts why an analysis of the phenotypic differences between the African and Asian lineages, as well as between the many strains, which have evolved under each branch, is a vital component of our ongoing effort to develop vaccines or therapeutics and fill major gaps of knowledge regarding ZIKV pathogenesis
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