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Brazil's Missing Infants: Zika Risk Changes Reproductive Behavior.

ABSTRACT: Zika virus epidemics have potential large-scale population effects. Controlled studies of mice and nonhuman primates indicate that Zika affects fecundity, raising concerns about miscarriage in human populations. In regions of Brazil, Zika risk peaked months before residents learned about the epidemic and its relation to congenital anomalies. This spatiotemporal variation supports analysis of both biological effects of Zika infection on fertility and the effects of learning about Zika risk on reproductive behavior. Causal inference techniques used with vital statistics indicate that the epidemic caused reductions in birth cohort size of approximately one-quarter 18 months after Zika infection risk peaked but 10 months after public health messages advocated childbearing delay. The evidence is consistent with small but not statistically detectable biological reductions in fecundity, as well as large strategic changes in reproductive behavior to temporally align childbearing with reduced risk to infant health. The behavioral effects are larger for more-educated and older women, which may reflect facilitated access to information and to family planning services within high-risk, mosquito-infested urban locations as well as perceptions about the opportunity costs of risks to pregnancy and infant survival.

SUBMITTER: Rangel MA

PROVIDER: S-EPMC7606566 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ImportanceA better pathophysiologic understanding of the neurodevelopmental abnormalities observed in neonates exposed in utero to Zika virus (ZIKV) is needed to develop treatments. The retina as an extension of the diencephalon accessible to in vivo microcopy with spectral-domain optical coherence tomography (SD-OCT) can provide an insight into the pathophysiology of congenital Zika syndrome (CZS).ObjectiveTo quantify the microstructural changes of the retina in CZS and compare these changes with those of cobalamin C (cblC) deficiency, a disease with potential retinal maldevelopment.Design, setting, and participantsThis case series included 8 infants with CZS and 8 individuals with cblC deficiency. All patients underwent ophthalmologic evaluation at 2 university teaching hospitals and SD-OCT imaging in at least 1 eye. Patients with cblC deficiency were homozygous or compound heterozygotes for mutations in the methylmalonic aciduria and homocystinuria type C (MMACHC) gene. Data were collected from January 1 to March 17, 2016, for patients with CZS and from May 4, 2015, to April 23, 2016, for patients with cblC deficiency.Main outcomes and measuresThe SD-OCT cross-sections were segmented using automatic segmentation algorithms embedded in the SD-OCT systems. Each retinal layer thickness was measured at critical eccentricities using the position of the signal peaks and troughs on longitudinal reflectivity profiles.ResultsEight infants with CZS (5 girls and 3 boys; age range, 3-5 months) and 8 patients with cblC deficiency (3 girls and 5 boys; age range, 4 months to 15 years) were included in the analysis. All 8 patients with CZS had foveal abnormalities in the analyzed eyes (8 eyes), including discontinuities of the ellipsoid zone, thinning of the central retina with increased backscatter, and severe structural disorganization, with 3 eyes showing macular pseudocolobomas. Pericentral retina with normal lamination showed a thinned (<30% of normal thickness) ganglion cell layer (GCL) that colocalized in 7 of 8 eyes with a normal photoreceptor layer. The inner nuclear layer was normal or had borderline thinning. The central retinal degeneration was similar to that of cblC deficiency.Conclusions and relevanceCongenital Zika syndrome showed a central retinal degeneration with severe GCL loss, borderline inner nuclear layer thinning, and less prominent photoreceptor loss. The findings provide the first, to date, in vivo evidence in humans for possible retinal maldevelopment with a predilection for retinal GCL loss in CZS, consistent with a murine model of the disease and suggestive of in utero depletion of this neuronal population as a consequence of Zika virus infection.

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Brazil's Missing Infants: Zika Risk Changes Reproductive Behavior.

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