Lais Takata Walter, Guilherme Shigueto Vilar Higa, Juliane Midori Ikebara, Danila Vedovello, Felipe Scassi Salvador, Silvia Honda Takada, Erika Reime Kinjo, Benjamin J Whalley, Márcia Aparecida Sperança, Alexandre Hiroaki Kihara
Journal: Molecular neurobiology 2018;55(2):1620-1629
PMID: 28190239
The Zika virus (ZIKV) outbreak that occurred in the northeast of Brazil in 2015 led to alarming numbers of babies born with microcephaly in this region. Since then, several studies have evaluated the relationship between ZIKV infection and development of the malformation although the specific mechanistic interaction between ZIKV and human physiological processes that ultimately manifest as microcephaly remains debated. Importantly, most current studies did not consider the specificities of the biology and life cycle of ZIKV. As a consequence, specificities of the infection on the developing central nervous system (CNS) were frequently disregarded. In order to begin to address this important gap in our knowledge, we have collated and critically reviewed the existing evidence in this area to identify any emerging consensus on this topic and thereafter describe possible mechanisms by which ZIKV infection could interfere with specific processes of CNS development, such as neuronal proliferation, and the complex interactions of immature neurons with radial glial cells. With this, we were able to present the current knowledge on this important topic in the neurobiology field.
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