Abstract
Zika virus (ZIKV) causes Congenital Zika Syndrome (CZS) in individuals exposed prenatally. Here, we investigated polymorphisms in VEGFA, PTGS2, NOS3, TNF, and NOS2 genes as risk factors to CZS. Forty children with CZS and forty-eight children who were in utero exposed to ZIKV infection, but born without congenital anomalies, were evaluated. Children with CZS were predominantly infected by ZIKV in the first trimester (p < 0.001) and had mothers with lower educational level (p < 0.001) and family income (p < 0.001). We found higher risk of CZS due the allele rs2297518[A] of NOS2 (OR = 2.28, CI 95% 1.17–4.50, p = 0.015). T allele and TT/CT genotypes of the TNF rs1799724 and haplotypes associated with higher expression of TNF were more prevalent in children with CZS and severe microcephaly (p = 0.029, p = 0.041 and p = 0.030, respectively). Our findings showed higher risk of CZS due ZIKV infection in the first trimester and suggested that polymorphisms in NOS2 and TNF genes affect the risk of CZS and severe microcephaly.
Highlights
Zika virus (ZIKV) is a human teratogen capable of causing neurological and ocular malformations in fetuses with in utero exposure to ZIKV infection [1,2]
Eighty-eight children who were in utero exposed to ZIKV infection were recruited for this study
Most mothers of children with Congenital Zika Syndrome (CZS) were exposed to ZIKV infection in the first trimester (80%) while most mothers of children without CZS were exposed to ZIKV infection the third trimester (44%) (p < 0.001)
Summary
Zika virus (ZIKV) is a human teratogen capable of causing neurological and ocular malformations in fetuses with in utero exposure to ZIKV infection [1,2]. The investigation of molecular changes caused by ZIKV during infection, such as in the gene expression, is one approach used to understand its molecular mechanisms and factors associated with its teratogenesis. Studies in this context have shown an exacerbated activity of genes/proteins involved in the immune and inflammatory response during ZIKV infection [7,8,9,10]
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