Maternal-fetal transmission of Zika virus and long-term neurodevelopmental outcomes in children: a narrative review

Introduction

The Zika virus (ZIKV), a member of the flavivirus family, is primarily transmitted through mosquito bites, particularly from female mosquitoes (1,2). Initially identified in 1947 in the Zika Forest of Uganda (3), it had spread across Asia by 1966 (4). While mosquitoes serve as the principal vector for ZIKV transmission (2), alternative transmission routes include sexual contact (5,6), blood transfusions (7), organ donation (8), and vertical transmission from mother to fetus (9). The first recorded human outbreak occurred on the island of Yap in 2007 (10), with predominant symptoms including rash, fever, conjunctivitis, and arthralgia, alongside milder symptoms such as headaches and myalgia (10). In 2015, Brazil reported between 440,000 and 1,300,000 probable ZIKV cases (11). This outbreak was followed by an increase in infants born with microcephaly in Brazil, suggesting a potential association between ZIKV infection and the condition (12). Congenital Zika syndrome (CZS) manifests in infants exposed to ZIKV during pregnancy via vertical transmission (13). Microcephaly, characterized by a head circumference below normal, is the most prevalent condition, occurring in approximately 80% of cases, with recent studies suggesting a prevalence of up to 91% (13,14). A recent comprehensive systematic review and meta-analysis in 2026 has revealed that ZIKV infection during pregnancy is associated with a pooled risk of CZS of 4.65% and a pregnancy loss rate of 2.48%, underscoring the clinical importance of vertical transmission (15). Additional cerebral abnormalities include cerebellar hypoplasia, ventriculomegaly, cortical deformities, and subcortical calcifications (14-16). Neurological issues such as hypertonia, rigidity, seizures, and irritability are also common (17), as are joint contractures (18,19) and auditory impairments (20,21). Furthermore, significant ocular abnormalities, including chorioretinal atrophy and pigment mottling, were observed in approximately 34% of infants with CZS and microcephaly (22,23). Human ZIKV infections (Figure 1) are generally self-limiting, presenting with general symptoms such as fever, headache, and myalgia (10). Pregnant women experience similar symptoms post-virus incubation, with rash being the most prevalent symptom, accompanied by mild fever and arthralgia (24). Despite the self-limiting nature of the virus, it can cross the placenta, leading to severe outcomes such as neurological disease, growth impairment, or fetal death (25). Several studies have identified the localization of ZIKV in Hofbauer cells (HCs), which are implicated in the transmission of infection to the fetus during the first trimester (26). However, other studies have proposed that neural stem and progenitor cells may also contribute to fetal neurological symptoms (27,28). Conversely, an increase in HCs was observed following viral infection, persisting for several months (29). The most common diagnostic method for infection is the enzyme-linked immunosorbent assay (ELISA) screening test, which may yield negative results but does not exclude the presence of an active infection (30). Reverse transcription polymerase chain reaction (RT-PCR) can detect the infection within the first week of onset. Urine samples, which contain the highest viral load, are preferable due to their longer viability compared to other samples and the reduced risk associated with non-invasive procedures (31).

Figure 1 Illustration of the Zika infection cycle and its impact on humans. ZIKV, Zika virus.

This narrative review aims to examine the complex interactions and implications of the ZIKV by exploring its background, transmission dynamics, complications, and future directions. We present this article in accordance with the Narrative Review reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0118/rc).

Methods

Study design and literature search strategy

This study was conducted as a narrative review with elements of a systematic approach to enhance comprehensive overview of the literature. An extensive electronic literature search was performed across three databases: Web of Science, PubMed, and Scopus.

The search strategy combined Medical Subject Headings (MeSH) terms and keywords as follows: (“Zika virus” AND “maternal-fetal transmission”) OR (“Zika virus” AND “congenital infection”) OR (“Zika virus” AND “neurological effects” AND “children”) OR (“Zika virus” AND “developmental outcomes”).

The search was limited to studies published between 2015 and 2024. The full search strategy is summarized in Table 1.

Inclusion and exclusion criteria

Studies included original research articles, particularly observational studies (cohort, case-control, and cross-sectional), as well as clinical trials and relevant review articles. Both retrospective and prospective studies were considered.

Inclusion criteria were: studies published in English, full-text availability, studies addressing maternal-fetal transmission of ZIKV and/or neurodevelopmental outcomes in children. Exclusion criteria included studies published before 2015, studies lacking original data, studies with insufficient or no follow-up data. To improve the interpretability of findings, a distinction was made between maternal exposure to ZIKV and confirmed congenital infection, as this may influence reported outcomes the distinction was in the present study, maternal exposure was defined as confirmed maternal infection during pregnancy based on [polymerase chain reaction (PCR)/serology/clinical diagnosis]. Confirmed congenital infection was defined as [neonatal PCR positivity/detection of immunoglobulin M (IgM)/clinical and radiological findings] within 10 days of birth.

Quality assessment

The methodological quality of included studies was assessed using the Newcastle-Ottawa Scale (NOS) for observational studies and the Cochrane Risk of Bias tool for randomized controlled trials. Additionally, heterogeneity in study design, sample size, and follow-up duration, as well as potential sources of bias, were considered during data interpretation.

ZIKV results

Following a comprehensive search of relevant databases and search engines, 21 citations were identified as pertinent to this narrative review. Each paper was evaluated and satisfied the inclusion criteria, thereby warranting their inclusion in this review. The research encompassed in these citations was published between 2016 and 2024. An overview of all included studies is presented in Table 2.

Discussion

The ZIKV is distinguished among pregnancy-associated infections by the specificity and severity of its effects on fetal neurodevelopment. In contrast to most other teratogenic viruses, which generally produce non-specific effects, ZIKV demonstrates a selective tropism for neural progenitor cells, resulting in a characteristic and reproducible pattern of brain injury that is most pronounced when maternal infection occurs during the first trimester. This discussion synthesizes evidence regarding vertical transmission mechanisms, the spectrum of neurodevelopmental consequences, and clinical management considerations, before evaluating the methodological quality of the included studies.

Mechanisms and determinants of vertical transmission

ZIKV primarily traverses the placenta via human decidual cells, which, instead of limiting viral replication, actively facilitate it, thereby enabling transmission to fetal tissues (1). This permissiveness is dependent on gestational age and is most pronounced during the first trimester, a period when fetal neural progenitor cells are particularly vulnerable, significantly increasing the risk of severe outcomes such as microcephaly and neural tube defects (2). Consequently, the placenta functions not as a passive barrier but as an active conduit for infection during early pregnancy. In addition to transplacental transmission, Porras-García et al. have demonstrated that delivery itself constitutes an additional transmission window, with ZIKV antibodies detected in neonatal saliva within hours of birth (37). Notably, the risk of transmission via breast milk is low, and breastfeeding is generally deemed safe in ZIKV-endemic regions (37). A diagnostically significant observation is that while the detection of ZIKV in body fluids such as amniotic fluid and urine confirms exposure, it does not reliably predict the severity of neurological sequelae, suggesting that host immune and genetic factors influence disease expression (3). Diagnosis is further complicated by the limited window of IgM detectability and the extensive serological cross-reactivity between ZIKV and other flaviviruses, highlighting the necessity for RT-PCR-based confirmation during pregnancy and the development of improved point-of-care diagnostics in endemic areas (Figure 2) (4).

Figure 2 Transmission routes of Zika virus and associated outcomes. The Zika virus is primarily transmitted by Aedes mosquitoes and can be detected in various body fluids. Sexual transmission during pregnancy may result in intrauterine infection and the development of CZS. Although viral RNA is present in breast milk, breastfeeding is not associated with CZS and may only lead to perinatal infection. The case of the second child highlights the distinction between congenital and perinatal outcomes and does not suggest transmission in subsequent pregnancies. CZS, congenital Zika syndrome.

Spectrum of neurodevelopmental consequences

CZS constitutes the most severe consequence of in utero exposure to the ZIKV. Although microcephaly, defined by a head circumference below the standard for gestational age and sex, is the hallmark and most recognizable feature of CZS, it is imperative to recognize that microcephaly is not the primary lesion. Rather, it is a secondary outcome of underlying cortical malformations and cerebral atrophy resulting from ZIKV’s disruption of neural progenitor cell proliferation and cortical development; the reduced head circumference indicates the brain’s failure to grow normally, rather than a primary skull abnormality. Consequently, microcephaly is neither the sole nor always the most clinically significant consequence of congenital ZIKV infection. Structural brain abnormalities, including ventriculomegaly, cortical atrophy, subcortical calcifications, and cerebellar hypoplasia, are consistently documented across cohort studies and may occur independently of microcephaly (5,35). Beyond the cranium, CZS also encompasses ocular abnormalities such as chorioretinal atrophy and optic nerve hypoplasia, joint contractures (arthrogryposis), and sensorineural hearing loss, reflecting the systemic reach of ZIKV infection during organogenesis (6). Importantly, the absence of microcephaly at birth does not preclude later neurological impairment. Research indicates that normocephalic ZIKV-exposed children may initially appear developmentally intact but subsequently develop motor difficulties, epilepsy, visual impairments, and language delays—a delayed-onset phenotype that necessitates prolonged clinical vigilance (7-9). This pattern suggests that ZIKV selectively disrupts neural connectivity in ways that may not be structurally apparent at birth but become functionally manifest as developmental demands increase during early childhood (Figure 3). Beyond structural abnormalities, ZIKV disrupts embryonic neurogenesis by infecting neural progenitor cells and triggering apoptosis, impairing the normal processes of neuronal proliferation, migration, and cortical organization (11). This molecular disruption gives rise to a broader range of neurological manifestations than microcephaly alone: affected children may develop epilepsy, motor dysfunction, encephalopathy, Guillain-Barré syndrome, and sensory neuropathy (10). Importantly, these sequelae are not confined to children with confirmed CZS. Do Amaral et al. [2021] documented developmental delays and motor impairments emerging months to years after birth in children who appeared normal at birth, emphasizing that any degree of in utero ZIKV exposure warrants sustained neurodevelopmental monitoring (12).

Figure 3 An analysis of the transmission and post-infection effects of the ZIKV during pregnancy and childbirth, utilizing data derived from prospective studies. It emphasizes the significant proportion of adverse outcomes observed among fetuses and neonates whose mothers were infected with ZIKV, as well as the potential risk of long-term consequences, such as neurodevelopmental delay. ZIKV, Zika virus.

Long-term neurodevelopmental outcomes and functional impairment

Longitudinal follow-up studies have demonstrated that the neurodevelopmental effects of congenital ZIKV exposure extend significantly beyond the neonatal period. Children diagnosed with CZS exhibit persistent impairments in motor, cognitive, and language domains at 12 and 24 months, suggesting that ZIKV continues to impact neurodevelopment beyond the initial insult (48). This trajectory indicates ongoing neurological dysfunction rather than a fixed, static injury, a distinction with direct implications for clinical management and the timing of therapeutic interventions. Emerging cellular evidence corroborates this interpretation: analyses of brain tissue from children with CZS reveal persistent neuroinflammation and synaptic dysfunction, indicating that ZIKV induces long-lasting disruption of neuronal connectivity extending beyond early developmental stages (49). Collectively, these findings challenge the model in which ZIKV causes a discrete perinatal event with finite consequences and instead support a framework of progressive neurological vulnerability necessitating long-term structured follow-up.

Prevention, early intervention, and clinical management

Given the extended and variable trajectory of neurodevelopmental outcomes following congenital ZIKV exposure, a multimodal and longitudinal approach to clinical management is imperative. Antenatal care should incorporate comprehensive ZIKV screening in endemic regions, with RT-PCR-based confirmation prioritized over serology alone to mitigate diagnostic uncertainty. For children with confirmed or suspected congenital infection, routine multidisciplinary neurodevelopmental assessments, including neurological, ophthalmological, audiological, and motor evaluations, should be initiated from birth and sustained through early childhood, irrespective of the presence of microcephaly at birth. Structured neurodevelopmental intervention programs have demonstrated measurable benefits: the randomized controlled trial by Waechter et al. [2022] reported significant improvements in language development and behavioral outcomes in 30-month-old ZIKV-exposed normocephalic children following a targeted intervention, underscoring the value of early support even in the absence of overt CZS signs (13). Vigilance must also be maintained in non-endemic settings, as imported cases and asymptomatic maternal infection may go unrecognized (14). Early identification and intervention before developmental deficits become entrenched offer the greatest prospect for improving long-term functional outcomes in affected children.

Critical appraisal of the evidence base

The 21 studies included in this review demonstrate significant methodological heterogeneity, encompassing experimental in vitro designs, cross-sectional surveys, prospective cohorts, a randomized controlled trial, and both narrative and systematic reviews. This diversity constrains formal meta-analytic synthesis and necessitates cautious qualitative interpretation. The majority of primary studies originated from Brazil during the 2015–2016 epidemic, raising concerns about generalizability to other endemic settings with differing healthcare infrastructure, co-circulating flaviviruses, and background seroprevalence, all of which impact diagnostic accuracy and observed outcome rates. Outcome measures were equally diverse: studies variously captured structural abnormalities at birth, functional neurodevelopmental domains at 12–36 months, and cellular-level neuropathology, employing different assessment instruments and follow-up intervals that preclude direct cross-study comparisons. Sample size limitations were prevalent: the sole randomised controlled trial (RCT) enrolled only 39 participants, and several observational studies did not report exact numbers, restricting statistical power and generalizability. Studies with longer follow-up extending to 24–36 months or beyond consistently identified delayed deficits absent in shorter-term studies, underscoring the critical importance of longitudinal surveillance and confirming that cross-sectional neonatal assessments substantially underestimate the true neurodevelopmental burden. Risk of bias was assessed using the NOS for observational studies and the Cochrane tool for the RCT; most studies achieved moderate scores (NOS 5–7/9), with recurring concerns including selection bias from enrollment of symptomatic-only cases, diagnostic misclassification from flavivirus serological cross-reactivity, unblinded outcome assessment, and attrition in low-resource cohorts. A fundamental methodological inconsistency throughout the literature is the conflation of maternal ZIKV exposure with confirmed congenital infection: studies that attributed adverse outcomes to ZIKV without neonatal diagnostic confirmation likely overestimated incidence, while those applying strict confirmatory criteria may underestimate burden where diagnostic capacity is limited. Addressing this distinction through standardized case definitions, RT-PCR-confirmed neonatal diagnoses, and harmonized long-term follow-up protocols represents the most important priority for strengthening the evidence base in future research.

Conclusions

This review demonstrates how the ZIKV can have a major impact on the brain development of fetuses and children. Particularly in the early stages of pregnancy, the virus can pass through the placenta and harm the developing brain. ZIKV can cause many neurological, sensory, and developmental issues, microcephaly is the most well-known consequence.

Crucially, the consequences extend beyond childhood. Even though they seem normal at birth, some children with CZS may experience delays in their language, motor, and cognitive abilities later in life. According to recent data, ZIKV may potentially result in long-term alterations in brain function, such as inflammation and nerve connection impairment.

For children exposed to ZIKV, long-term monitoring, early screening, and early intervention are therefore crucial to enhancing their developmental outcomes and lowering the risk. Particularly in the early stages of pregnancy, the virus can pass through the placenta and harm the developing brain. ZIKV can cause many neurological, sensory, and developmental issues, however microcephaly is the most well-known consequence. Capacities can be mitigated, thereby offering affected families a greater prospect of achieving a healthy life.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0118/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0118/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-1-0118/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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