ABSTRACT
INTRODUCTION: The SARS-CoV-2 (COVID-19) pandemic was managed with sustained mass lockdowns to prevent spread of COVID-19 infection. Babies born during the early stages of the pandemic missed the opportunity of meeting a normal social circle of people outside the family home. METHODS: We compared 10 parentally reported developmental milestones at 12-month assessment in a cohort of 309 babies born at the onset of the pandemic (CORAL cohort) and 1629 babies from a historical birth cohort (BASELINE cohort recruited between 2008 and 2011). RESULTS: Compared with a historical cohort, babies born into lockdown appeared to have some deficits in social communication. Fewer infants in the pandemic cohort had one definite and meaningful word (76.6% vs 89.3%), could point (83.8% vs 92.8%) or wave bye-bye (87.7% vs 94.4%) at 12-month assessment. Adjusted log-binomial regression analyses demonstrated significant differences in social communication in the CORAL cohort compared with the BASELINE cohort: one definite and meaningful word (relative risk (RR): 0.86 (95% CI: 0.80 to 0.92)), pointing (RR: 0.91 (95% CI: 0.86 to 0.96)) and waving bye-bye (RR: 0.94 (95% CI: 0.90 to 0.99)). DISCUSSION: Parentally reported developmental outcomes in a birth cohort of babies born into lockdown during the COVID-19 pandemic may indicate some potential deficits in early life social communication. It must be noted that milestones are parentally reported and comparison is with a historical cohort with associated limitations. Further studies with standardised testing is required to validate these findings. CONCLUSION: Pandemic-associated social isolation may have impacted on the social communication skills in babies born during the pandemic compared with a historical cohort. Babies are resilient and inquisitive by nature, and it is hoped that with societal re-emergence and increase in social circles, their social communication skills will improve.
ABSTRACT
Autism spectrum disorder (ASD) is the commonest neurodevelopmental disability. It is a highly complex disorder with an increasing prevalence and an unclear etiology. Consensus indicates that ASD arises as a genetically modulated, and environmentally influenced condition. Although pathogenic rare genetic variants are detected in around 20% of cases of ASD, no single factor is responsible for the vast majority of ASD cases or that explains their characteristic clinical heterogeneity. However, a growing body of evidence suggests that ASD susceptibility involves an interplay between genetic factors and environmental exposures. One such environmental exposure which has received significant attention in this regard is maternal immune activation (MIA) resulting from bacterial or viral infection during pregnancy. Reproducible rodent models of ASD are well-established whereby induction of MIA in pregnant dams, leads to offspring displaying neuroanatomical, functional, and behavioral changes analogous to those seen in ASD. Blockade of specific inflammatory cytokines such as interleukin-17A during gestation remediates many of these observed behavioral effects, suggesting a causative or contributory role. Here, we review the growing body of animal and human-based evidence indicating that interleukin-17A may mediate the observed effects of MIA on neurodevelopmental outcomes in the offspring. This is particularly important given the current corona virus disease-2019 (COVID-19) pandemic as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during pregnancy is a potent stimulator of the maternal immune response, however the long-term effects of maternal SARS-CoV-2 infection on neurodevelopmental outcomes is unclear. This underscores the importance of monitoring neurodevelopmental outcomes in children exposed to SARS-CoV-2-induced MIA during gestation.