Marques Fernanda J P, Ruan Janet, Razal Rozel B, Leyser Marcio, Kousa Youssef A
SARAH Network of Rehabilitation Hospitals, Rio de Janeiro, Brazil.
Developmental and Behavioral Pediatrics, Stead Family Department of Pediatrics, University of Iowa Health Care, Iowa City, IA, USA.
Pediatr Res. 2025 Jul 1. doi: 10.1038/s41390-025-04252-1.
The severity of virally induced prenatal brain injury, even among dizygotic twins, varies according to individual and maternal risk and protective factors, including genomics.
This scoping review aims to analyze data on genetic susceptibility to neurological outcomes in children exposed in utero to Zika virus.
We followed JBI methodology for this scoping review. A search in PubMed, Scopus, CINAHL, Web of Science, Academic Search Ultimate, Agricola, Health Source: Nursing/Academic Edition, and Psychology and Behavioral Sciences Collection was conducted. Three reviewers independently screened studies using the Rayyan platform. Studies on gene mutations impacting brain injury after Zika virus infection were included.
Thirteen articles identifying candidate genes related to brain injury were reviewed. Twenty-three genes were implicated in modulating susceptibility to prenatal brain injury, including six maternal and 17 infant genes.
Maternal and fetal genetic factors likely contribute susceptibility to virally induced prenatal brain injury. Analyzing polygenic risk could aid in future screening programs to identify individuals at risk. This information may eventually be integrated into clinical data, helping healthcare providers, families, and patients understand how to personalize care for better outcomes.
This paper evaluates available evidence about the relationship between genetic susceptibility and neurological consequences of Zika virus exposure during pregnancy. After performing a scoping review, we identified 13 articles describing candidate genes that potentially contribute to the development of virally induced brain injury after prenatal Zika infection. Of the genes identified, six were associated with maternal risks, while 17 were linked to the fetus. Maternal and prenatal genetic factors could increase the risk of virally induced prenatal brain injury. Future research should investigate factors that can modify disease pathogenesis toward the goal of reducing the global impact of brain injury.
即使在异卵双胞胎中,病毒引起的产前脑损伤的严重程度也因个体和母体的风险及保护因素(包括基因组学)而异。
本范围综述旨在分析子宫内接触寨卡病毒的儿童发生神经学结局的遗传易感性数据。
我们遵循JBI方法进行本范围综述。在PubMed、Scopus、CINAHL、Web of Science、Academic Search Ultimate,、Agricola、Health Source: Nursing/Academic Edition和Psychology and Behavioral Sciences Collection中进行了检索。三名评审员使用Rayyan平台独立筛选研究。纳入了关于寨卡病毒感染后影响脑损伤的基因突变的研究。
对13篇鉴定与脑损伤相关候选基因的文章进行了综述。23个基因与调节产前脑损伤易感性有关,包括6个母体基因和17个婴儿基因。
母体和胎儿遗传因素可能导致病毒引起的产前脑损伤易感性。分析多基因风险有助于未来的筛查计划识别有风险的个体。这些信息最终可能会整合到临床数据中,帮助医疗保健提供者、家庭和患者了解如何进行个性化护理以获得更好的结果。
本文评估了关于孕期接触寨卡病毒的遗传易感性与神经学后果之间关系的现有证据。在进行范围综述后,我们确定了13篇描述可能导致产前寨卡感染后病毒引起的脑损伤发展的候选基因的文章。在鉴定出的基因中,6个与母体风险相关,17个与胎儿相关。母体和产前遗传因素可能增加病毒引起的产前脑损伤的风险。未来的研究应调查可改变疾病发病机制的因素,以减少脑损伤的全球影响为目标。