Across studies of socio-emotional and behavioral development (16-28), there was a consistent pattern of elevated difficulties among children exposed to the COVID-19 pandemic period, with evidence from meta-analyses indicating a higher prevalence of emotional and behavioral problems compared with pre-pandemic estimates (11,14). Additionally, longitudinal cohorts documented increases in emotional and peer problems over time, with changes observed from the pre-pandemic period (2018-2019) through the early pandemic phase (2020) and into later phases (2021-2022) (15). A subset of children followed persistent high-symptom trajectories across the pandemic period, particularly in emotional and oppositional-defiant domains (16). These trajectories were strongly shaped by family-level stressors, including elevated parental psychological distress, job or income loss, increased caregiving burden and disruptions to daily routines. Such family-level stressors were central to the observed patterns as they reduced the emotional and regulatory resources available within the family environment, thereby heightening children's vulnerability to socio-emotional difficulties during periods of prolonged uncertainty and disruption. Broader caregiver stressors, such as financial strain, household chaos, reduced childcare access and pandemic-related disruptions, were consistently associated with increases in children's internalizing symptoms (for example, anxiety and withdrawal) and externalizing symptoms (for example, irritability and aggression), sleep problems and behavioral dysregulation (17-19), with longitudinal evidence indicating stronger associations in families with less socioeconomic resources (15).

Among infants and toddlers, higher maternal depression and anxiety, increased parenting stress, reduced social support, and disrupted daily routines were associated with increased socio-emotional difficulties (20,29,30). Peer difficulties increased in preschoolers during the pandemic, with positive parent-child interactions buffering these effects, although these supports did not consistently mitigate emotional symptoms, which remained associated with caregiver stress and broader household disruptions (15,16,29). Despite these patterns, findings were not uniform. A number of studies reported relatively consistent socio-emotional functioning when family routines were preserved or when parental mental health remained stable (31,32). In addition, the magnitude of socio-emotional difficulties varied across cultural and policy contexts, where strict lockdowns, extended preschool closures and culturally specific caregiving patterns, such as reliance on structured early education in Germany and prolonged home confinement with limited outdoor play in China, were associated with more pronounced effects in settings experiencing prolonged lockdowns or greater household disruption (17,19). In these studies, household disruption referred to increased parental stress, job or income loss, crowded or unstable living arrangements and significant disturbances to daily routines. These variations highlight the importance of contextual factors in shaping the socio-emotional responses of children to pandemic-related stress. However, interpretation of these findings was constrained by numerous methodological limitations, including reliance on parent-reported measures, convenience sampling, heterogeneous exposure definitions and notable attrition in longitudinal cohorts. Therefore, caution is warranted when interpreting the magnitude of socio-emotional differences, even though the overall pattern of increased vulnerability remained consistent.

Across studies examining cognition, language and EF development (12,13,33-45), a number of points of convergence emerged regarding the developmental consequences of the COVID-19 pandemic for infants and young children. Firstly, modest but consistent reductions across communication, problem-solving and personal-social domains were observed across numerous large-scale and international cohorts (33,46), with communication and problem-solving demonstrating the clearest disruptions (14,33,46). Furthermore, a number of studies reported increased probabilities of screening positive for developmental delay, which was driven in part by increased rates of language-specific delays (34-36). However, these patterns were not uniform across all children, as preterm (gestational age <32 weeks) or very low birth weight (<1,500 g) infants exhibited the most pronounced differences, with notably lower cognitive and language scores compared with pre-pandemic peers (37). Although these infants represented a subgroup that was biologically at-risk due to immature brain development, higher rates of neonatal complications and increased vulnerability to environmental stressors, their developmental profiles were consistent with broader international findings, which indicated small but reliable reductions in early problem-solving and communication abilities among pandemic-born infants (14), as well as early delays in social communication, including reduced meaningful word use, pointing and waving (38). Converging findings from cohort studies and a comprehensive review of international research documented consistent patterns of lower performance in morphosyntax, expressive vocabulary, phonological awareness and early literacy skills, with instructionally dependent language skills having the largest disruptions and children from lower socioeconomic backgrounds having the longest delays (12,39,40). Teacher-reported longitudinal data, analyzed in a study by Bub et al (47), indicated that early learning and social-emotional skills were shaped by the quality of remote learning supports, with marginalized children receiving a reduced number of resources and less frequent teacher contact. These population-level shifts were moderated by parental mental health and early-education environments, in which maternal depression amplified developmental delays, whereas higher-quality early care settings were associated with more favorable outcomes, including enhanced expressive vocabulary, better early literacy skills and more advanced socio-emotional competencies.

A second area of consistent convergence was the role of caregiver psychological functioning. Across diverse cohorts, prenatal psychological distress, measured through mental health symptoms, pandemic-related stress or reduced social support, consistently predicted less optimal infant socio-emotional, regulatory and socio-cognitive outcomes, often operating indirectly through postnatal maternal mental health and parenting stress (20-22,29,30). Postnatal maternal depression, anxiety and perceived stress had similar associations, and a systematic review identified associations between postnatal depression and poorer mother-infant bonding, alongside difficulties in infant motor, self-regulation and socioemotional development (23). Furthermore, individual cohorts demonstrated that higher maternal stress predicted increased infant crying, fussiness and regulatory challenges even after accounting for prenatal symptoms (24,29). In addition, early motor development had a similar sensitivity to maternal mental health; higher prenatal and postpartum depressive symptoms were associated with poorer neonatal fine and gross motor abilities, with the strongest effects observed among preterm and low-birth-weight infants (25,33). Population-level data in studies by Giesbrecht et al (48) and Perrigo et al (46) also demonstrated these patterns as large municipal and national datasets showed that children exposed to the pandemic exhibited developmental lags by preschool age, with widening variability in developmental outcomes. These population-level shifts were moderated by family mental health and early-education environments (26,47,49). Taken together, these findings suggested that pandemic-related disruptions influenced not only mean levels of development but also the distribution and heterogeneity of developmental functioning across cohorts.

Despite these areas of convergence, a number of divergences were noted. Studies examining the impact of maternal severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during pregnancy yielded mixed results. Certain studies reported elevated developmental risk, particularly when infection occurred in the first or second trimester, was severe or co-occurred with prematurity (34,35,37). However, other studies found no association between prenatal infection and developmental outcomes (41-43). These discrepancies may reflect differences in illness severity, timing of exposure, sample characteristics and measurement tools, a pattern consistent with broader heterogeneity across pandemic-era cohorts. Additionally, findings regarding motor development varied across studies, as although a number identified delays, particularly among high-risk infants or in the context of maternal mental health difficulties (25,37,44), a large population-based study reported no pandemic-related differences in gross motor (namely, walking without assistance and climbing stairs with assistance) and fine motor (namely, building a tower of cubes) milestones at 2 years of age (45).

EF-related processes (for example working memory, inhibitory control, cognitive flexibility) also appeared particularly sensitive to these stress-related and environmental disruptions (13,24,50-53). A quasi-experimental study from Russia found that preschoolers assessed during lockdown showed slower gains in cognitive flexibility and working memory, while inhibitory control remained relatively stable; girls had increased attenuation in working-memory development, suggesting potential sex-based differences in sensitivity to disrupted routines (13). Other studies also documented EF-related disruptions. In preschoolers, working memory mediated associations between environmental routines and emotional dysregulation (51) and studies of infant regulatory behaviors showed that maternal stress and reduced social support were associated with poorer early regulatory capacity (24,52), an EF-precursor skill (53). Additional studies reported increased difficulties regarding attentiveness and distractibility in the context of family stress, disrupted routines or harsh parenting, defined as punitive, irritable or overreactive disciplinary practices measured using the Parenting Scale and the inconsistent-discipline items of the Alabama Parenting Questionnaire (18,27), reinforcing the role of early stress and environmental instability in shaping EF-related pathways. Collectively, these findings indicated that while cognitive and language disruptions during the pandemic were modest, EF processes had an increased sensitivity to stress-related and environmental instability, highlighting the role of caregiver wellbeing and daily routines in shaping early developmental trajectories.

Taken together, this evidence indicated that the COVID-19 pandemic exerted broad but heterogeneous influences on early development. The most consistent patterns suggested modest population-level shifts in communication and socio-cognitive domains (33,46,54), increased vulnerabilities among biologically or socioeconomically at-risk infants (12,37), and robust pathways that associate caregiver psychological functioning with infant outcomes (39,47). Divergences across studies, particularly regarding prenatal infection and motor development, highlights the need for continued longitudinal follow-up and harmonized assessment approaches.

However, the interpretation of these findings is affected by a number of methodological limitations across these cognition, language and EF studies. The majority of cohorts relied on parent-reported screening tools, such as the Ages and Stages Questionnaire-3, which are sensitive to parental stress and reporting bias (55) and may not detect subtle cognitive or language differences (56). Numerous samples were convenience-based, highly educated or lacked socioeconomic and racial diversity, limiting generalizability. Exposure definitions also varied widely, from broad pandemic-period indicators to specific measures of maternal infection or family stress, complicating comparisons across studies. Studies investigating maternal SARS-CoV-2 infection often included mild or asymptomatic cases, reducing the ability to detect the effects of more severe illness. Follow-up periods were frequently short, particularly for infants assessed in the first year of life, leaving uncertainty regarding whether early differences persist or resolve over time. Taken together, due to these limitations, caution in interpreting the magnitude of cognitive and language differences is suggested, even though the overall pattern indicated modest disruptions associated with contextual, as opposed to viral, exposures.

Across studies examining biological embedding during the COVID-19 pandemic, findings indicate subtle yet marked alterations in infant and child stress-related biology, though effects vary across biomarkers, tissues and exposure definitions (31,54,57-61). An epigenetic study reported pandemic-related differences in DNA methylation of stress-regulatory genes. Infants exposed in utero exhibit altered methylation in nuclear receptor subfamily 3 group C member 1 and solute carrier family 6 member 4 (SLC6A4), with trimester-specific patterns suggesting that first-trimester exposure may represent a particularly sensitive window of vulnerability (57). Genome-wide comparisons of pandemic-exposed neonates with pre-pandemic controls identifies hundreds of differentially methylated sites enriched in neurodevelopmental pathways (synapse organization, neurogenesis and axon guidance) and immune pathways (cytokine-mediated signaling, interferon responses and leukocyte activation), whereas maternal SARS-CoV-2 infection itself is not associated with methylation differences (58). By contrast, severe maternal infection is associated with widespread differential DNA methylation in infants and elevated maternal IL-6 concentrations, reflecting a heightened inflammatory milieu during pregnancy. These biological alterations show modest, domain-specific associations with developmental scores at 12 months, suggesting that maternal immune activation may exert subtle but measurable influences on early neurodevelopment (59,61). Additional research shows that higher prenatal pandemic-related stress predicts increases in infant SLC6A4 methylation, which is associated with altered temperament at 3 months (60).

Neuroimaging studies provide converging evidence that prenatal stress is associated with early alterations in infant brain structure and connectivity (54,62). Increased prenatal maternal anxiety predicts reduced left amygdala volumes at 3 months, which are subsequently associated with increased negative affectivity at 6 months (54). Complementary work shows that greater prenatal maternal distress is associated with altered infant white-matter microstructure and altered amygdala-prefrontal connectivity, suggesting early deviations in neural circuits supporting emotional regulation (62). Taken together, these findings offer preliminary evidence that prenatal stress during the pandemic may be associated with early structural and connectivity in neural systems implicated in emotion processing and regulation.

Physiological biomarkers showed a heterogeneous pattern as opposed to a uniform rise in stress physiology during the pandemic. In a small prenatal cohort, prenatal COVID-19-related stress was not associated with maternal hair cortisol concentrations (HCC), although socioeconomic status moderated this pattern, with a stress-cortisol association emerging only among women with a higher socioeconomic status; maternal HCC did not predict infant temperament (31). In a separate pre- to post-pandemic cohort with repeated hair-steroid assessments, mean levels of cortisol, cortisone and related adrenal steroids, such as dehydroepiandrosterone and dehydroepiandrosterone sulfate, did not change across the pandemic onset. However, family income and parent-reported family functioning (conflict resolution, cohesion and COVID-19-related stress) moderated these patterns, with increases in child HCC occurring primarily in households with lower income or greater family stress, with social support buffering these rises (61). Children with higher pre-pandemic morning basal salivary cortisol showed greater physiological reactivity, exhibiting steeper increases in anger when exposed to harsh or inconsistent parenting, but the lowest anger level when exposure to such parenting was low. Harsh or inconsistent parenting was defined as more punitive, irritable or unpredictable disciplinary practices measured using the Parenting Scale and the inconsistent-discipline subscale of the Alabama Parenting Questionnaire, both validated parent-report instruments (27). Collectively, these findings suggest a possible biological-sensitivity-to-context interpretation, in which individual differences stress physiology heighten vulnerability in adverse environments but are buffered in supportive ones, rather than reflecting a population-wide increase in cortisol.

Taken together, these findings suggest preliminary evidence of possible biological embedding associated with prenatal and early-life stress during the pandemic. However, interpretation of this evidence is constrained by numerous methodological limitations. The majority of studies relied on peripheral tissues (buccal cells, saliva and hair), which may not capture central nervous system processes. Sample sizes were small to modest, reducing the statistical power to detect subtle effects and increasing the likelihood of false positives in genome-wide analyses. Furthermore, the majority of cohorts lacked pre-pandemic biological baselines, making it difficult to isolate pandemic-specific effects. Additionally, exposure definitions varied widely between studies, from broad pandemic timing to specific measures of maternal stress or infection, which complicates comparability across studies. Samples were also often highly educated and socioeconomically advantaged, limiting generalizability. In addition, neuroimaging studies were restricted to single time points, preventing assessment of developmental trajectories. Finally, the observational nature of all studies suggests the possibility of residual confounding from unmeasured prenatal or postnatal factors. These limitations highlight the need for cautious interpretation, even though the emerging evidence indicates potential biological embedded effects of prenatal stress during the pandemic.