ZIP 2.0 STUDY CHILD COHORT WITH INTERIM ANALYSIS OF AGE 30 MONTHS DATA

点击翻译按钮获取中文摘要

Zika virus (ZIKV) is an arbovirus (vector-borne virus) of the genus Flaviviridae. Infections were thought to be mild and self-limiting until 2015, when an epidemic was observed initially in Brazil of microcephaly and other birth defects in newborns following infection of the mother during pregnancy with Zika virus (ZIKV). Increasing evidence now points to ZIKV as the agent responsible for a variety of birth defects in newborns of mothers who become infected during pregnancy. The relationship of ZIKV infections in pregnant women with adverse outcomes of pregnancy is the subject of ongoing evaluation. Studies to date of infants born to infected women focus on those born with serious birth defects that constitute the congenital Zika syndrome (CZS). Whether there are latent effects on growth and development in infants who are born without CZS to Zika-infected women, and what those effects may be, is unclear. Longitudinal studies of infants born to Zika-infected pregnant women are needed to assess the broader spectrum and natural history of possible manifestations of intrauterine or intrapartum Zika exposure. In 2016, NIH initiated a large, multicenter, international observational study of the epidemiology, natural history, and pathogenesis of Zika in infants and pregnancy (the ZIP Study). The ZIP Study followed infants born to women at risk for Zika infection during pregnancy only through the infants’ first 12 months of life and completed its last patient last visit December 2019. In 2018, NIH initiated the ZIP 2.0 cohort study of Zika exposed children and unexposed control children from the ZIP Study or similar studies, following children beyond infancy to 42 months of age to evaluate the effects of Zika on child growth and development. Recent studies have found that infants who had in utero ZIKV exposure without CZS appear to be at risk for abnormal neurodevelopmental outcomes in the first 18 months of life1 and similarly observed high frequencies of anatomical and neurodevelopmental abnormalities in children without microcephaly who were exposed to ZIKV in utero2. One study found a gradient of risk of development delay according to head circumference, with severely microcephalic children at highest risk for delays while normocephalic ZIKV-exposed children showed similar risk to unexposed control children3. However, several other studies have observed abnormal neurodevelopment in the absence of microcephaly among children with intrauterine ZIKV exposure4,5. Those reports indicate that nearly all such children presented at least one developmental delay and that a significant proportion of children exposed in utero to ZIKV developed mild cognitive delay and auditory behavioral abnormalities.