Neurology Central

Zika virus: where are we now?

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Zika virus: A public health emergency

On 1 February 2016, the World Health Organization (WHO) declared Zika virus (ZIKV) a “public health emergency of international concern”.   ZIKV is a flavivirus transmitted by the Aedes aegypti and Aedes albopictus mosquitoes. Since 2015, there has been a dramatic increase in countries reporting local transmission, with a total of 84 countries and territories reporting, to date [1]. The scientific and medical community rapidly rose to the challenge and launched a full-scale intervention in response to the WHO’s declaration. Everyone from public health officials to basic science researchers pulled resources to tackle the pandemic. Thanks to these efforts, the WHO announced on 18 November 2016 ZIKV was no longer a public health emergency. However, the virus continues to be a critical concern due to the associated neurological and developmental risks, as well as transmission patterns that still surprise us. While there are many questions that must be resolved, impressive strides have been made in the past year and half. This article will briefly address several of those advancements, and look toward the future of ZIKV research and treatment.

Zika models

The causal link between microcephaly and ZIKV infection was confirmed in 2016, as well as the capability of ZIKV to be transmitted by mosquito bites, sexual contact and contact with other bodily fluids [2]. This past July, a study from the University of Wisconsin (WI, USA) demonstrated ZIKV could undergo oropharyngeal mucosal transmission [3].

We know there are two primary lineages of ZIKV, African and Asian; however, to date, only Asian lineage strains are associated with microcephaly [4]. A seminal study by Waldorf and colleagues demonstrated a causal link between subcutaneous inoculation of pregnant non-human primates with ZIKV and development of fetal brain lesions [5]. However, financial and ethical constraints necessitate that most work be conducted in rodent models. Wu and colleagues showed that ZIKV can be vertically transmitted from mother to fetus and result in cortical development deficits [6]. Another study conducted by Cugola demonstrated that there was a significant upregulation in genes associated with autophagy and apoptosis following fetal infection [7]. This suggests that dysregulation of autophagy and increased cell death during development may cause ZIKV-associated defects [7]. To better address the pathophysiology of ZIKV in rodent models, Rossi and colleagues developed a novel murine model [8]. This transgenic mouse is deficient in interferon-alpha receptor and has an age-dependent response to ZIKV infection, which may prove beneficial in testing drugs at various developmental stages. Similar to humans, this mouse also harbors ZIKV in testis, making it an optimal model to study sexual transmission [8].

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