Abstract
Five years after the identification of Zika virus as a human teratogen, we reviewed the early clinical manifestations, collectively called congenital Zika syndrome (CZS). Children with CZS have a very poor prognosis with extremely low performance in motor, cognitive, and language development domains, and practically all feature severe forms of cerebral palsy. However, these manifestations are the tip of the iceberg, with some children presenting milder forms of deficits. Additionally, neurodevelopment can be in the normal range in the majority of the non-microcephalic children born without brain or eye abnormalities. Vertical transmission and the resulting disruption in development of the brain are much less frequent when maternal infection occurs in the second half of the pregnancy. Experimental studies have alerted to the possibility of other behavioral outcomes both in prenatally infected children and in postnatal and adult infections. Cofactors play a vital role in the development of CZS and involve genetic, environmental, nutritional, and social determinants leading to the asymmetric distribution of cases. Some of these social variables also limit access to multidisciplinary professional treatment.
Highlights
The Zika Virus (ZIKV) was first identified in monkeys in Uganda in 1947, and later in humans, it has received little attention since the clinical manifestations of its infection was comparatively mild relatively to other flavivirus, notably yellow fever and dengue viruses (Macnamara, 1954)
In those studies in which descriptions of the physical and neuroimaging phenotypes are thorough, including case control studies, two groups of children were identified. Those exposed to ZIKV in utero that did not have any abnormal phenotypic physical or neurologic findings, and those that had severe and complex physical and neurological phenotypes with devastating consequences for later development, a spectrum which was called the Congenital Zika syndrome (Moore et al, 2017; del Campo et al, 2017)
In the absence of definitive laboratory diagnostic tests, we emphasize the importance of the clinical/ epidemiological suspicion of congenital Zika syndrome (CZS), based on thorough dysmorphologicaland neurological examinations, brain images, and visual evaluations associated in individuals living or travelling to countries where ZIKV is circulating
Summary
The Zika Virus (ZIKV) was first identified in monkeys in Uganda in 1947, and later in humans, it has received little attention since the clinical manifestations of its infection was comparatively mild relatively to other flavivirus, notably yellow fever and dengue viruses (Macnamara, 1954). In late 2015, the consequences of prenatal infection by the Zika virus were suspected based on the occurrence of a cluster of children born with microcephaly in Northeast Brazil (França et al, 2016; Schuler-Faccini et al, 2016). The five major components of the phenotype used to define CZS were external physical dysmorphic features, a pattern of neurologic anomalies, joint contractures, neuroimaging findings, and ocular and hearing abnormalities (Moore et al, 2017; del Campo et al, 2017). We review the phenotypes associated with prenatal ZIKV infection and the neurodevelopment in these affected children. We cover the experimental data about the cellular and molecular mechanisms underlying these clinical outcomes
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