Neurological manifestations of Zika virus infection

Abstract

Zika virus (ZIKV) is a flavivirus (Flaviviridae family) transmitted mainly by Aedes mosquitoes. The virus was restricted to the African continent until its spread to south-east Asia in the 1980's, the Micronesia in 2007, the French Polynesia in 2013 and, more recently in the Americas in 2015, where, up to date, the World Health Organization (WHO) has estimated about 3-4 million total cases of ZIKV infection. During outbreaks in the French Polynesia and Brazil in 2013 and 2015, respectively, national health authorities reported potential neurological complications of ZIKV disease, chiefly an upsurge in Guillain-Barré syndrome, which coincided with ZIKV outbreaks. On the other hand, the emergence of ZIKV in Brazil has been associated with a striking increase in the number of reported cases of microcephaly in fetus and newborns, twenty times higher than in that reported in previous years. While investigations are currently assessing whether there is an actual association between neurological complications and ZIKV infections, the evidence was enough worrisome for WHO to declare a public health emergency of international concern. Here we present an updated review addressing what is currently known about the possible association between ZIKV infection and the development of severe neurological disorders.

Keywords: Flavivirus; Guillain-Barré syndrome; Microcephaly; Transmission routes; Zika virus.

Figure 1

Schematic representation of Zika virus genome organization. The single open reading fram (boxes) that encodes both structural and non-structural proteins is flanked by two untranslated regions.

Figure 2

Schematic representation of Zika virus particle based on cryo-electron microscopy data[4].

Figure 3

Schematic representation of Zika virus transmission cycle, with a sylvatic natural cycle between mosquitoes and monkeys, and an urban cycle between mosquitoes and human population.