Abstract
Prenatal viral infection can lead to a spectrum of neurodevelopmental disabilities or fetal demise. These can include microencephaly, global developmental delay, intellectual disability, refractory epilepsy, deafness, retinal defects, and cortical-visual impairment. Each of these clinical conditions can occur on a semi-quantitative to continuous spectrum, from mild to severe disease, and often as a collective of phenotypes. Such serious outcomes result from viruses’ overlapping neuropathology and hosts’ common neuronal and gene regulatory response to infections. The etiology of variability in clinical outcomes is not yet clear, but it may be related to viral, host, vector, and/or environmental risk and protective factors that likely interact in multiple ways. In this perspective of the literature, we work toward understanding the causes of phenotypic variability after prenatal viral infections by highlighting key aspects of the viral lifecycle that can affect human disease, with special attention to the 2015 Zika pandemic. Therefore, this work offers important insights into how viral infections and environmental teratogens affect the prenatal brain, toward our ultimate goal of preventing neurodevelopmental disabilities.
Highlights
Prenatal infections are a leading cause of 2.6 million neonatal deaths globally each year
Prenatal viral infections tend to cause the same types of neuropathology and neurodevelopmental disorders in a clinical continuum that can include microencephaly, global developmental delay, intellectual disability, refractory epilepsy, deafness, retinal defects, and cortical-visual impairment
The change in the mosquito population was a major factor in the pathogenesis of Zika virus, and other flaviviruses
Summary
Prenatal infections are a leading cause of 2.6 million neonatal deaths globally each year. Because of the number of people who were infected and are affected and mobilization by national and international research centers and funders to study this global health problem [22,23], the 2015 Zika virus pandemic offers a unique opportunity to study causes. The following sections cover differences in the virus, mosquito vector, human host, and their context, including public health and medical infrastructure, local community, and broader environment that can affect disease outcome after prenatal viral infection (Figure 2). In mouse models, adapted viral strains result in similar developmental defects with prenatal [39,40,41,42,43,44,45,46,47,48,49,50,51,52] or postnatal infection [24,53]
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