Zoonoses account for the majority of recognized mammalian viral spillover events, primarily originating from bats, rodents, and primates. Human activities have significantly accelerated these transmissions. This narrative review synthesizes the evolutionary, ecological, pathogen-related, and anthropogenic drivers of viral zoonotic spillover to identify critical leverage points for pandemic prevention. A narrative literature review was conducted. The analysis focused on factors enabling animal pathogens to transform into human pathogens, examining host species, pathogen traits, human–animal interactions, and environmental impacts. Pathogen transformation depends on host traits, contact frequency, and viral characteristics. Anthropogenic drivers—including livestock expansion, the bushmeat trade, wet markets, and the exotic pet industry—significantly elevate spillover risks. Effective pandemic prevention requires targeted interventions at the wildlife–livestock–human interfaces. A holistic, multidisciplinary collaboration between national governments and international organizations is essential to mitigate future risks.

Neonatal defense against pathogens relies on maternal antibodies transferred both through the placenta (IgG) and through breast milk (primarily secretory IgA). Maternal IgG antibodies are transferred across the placenta to the fetus mainly via the neonatal Fc receptor (FcRn), which is expressed at high levels in placental syncytiotrophoblasts, and results in the acquisition of maternal-fetal IgG. Transplacental transfer via the FcRn pathway can provide therapeutic proteins and protective antibodies following maternal vaccination. However, maternal IgG antibodies can bind to vaccine antigens such as measles, tetanus, and poliovirus, resulting in rapid clearance through FcgRIIB-mediated inhibition and inadequate B cell activation. In this way, they can inhibit de novo immune responses and significantly reduce vaccine response. On the other hand, the interference that breast milk-derived antibodies may have on vaccine-induced immunity is still largely unknown. Vaccination against influenza, pertussis, and COVID-19 during pregnancy or lactation has been shown to induce the production of protective, pathogen-specific, secretory IgA and IgG antibodies in breast milk. Conversely, studies found that breast milk-derived antibodies of vaccinated mothers reduced vaccine-induced immunity in breastfed infants by accelerating the clearance of vaccine antigen, resulting in reduced antigen availability and reduced plasma cell formation after vaccination. Additional factors in middle- and low-income countries, including environmental (increased microbiome diversity, environmental intestinal dysfunction, malnutrition, co-infections) and breastfeeding practices, may exacerbate the interference effect of maternal antibodies. Current evidence supports that breastfeeding is associated with a reduced immunological response exclusively to the rotavirus vaccine. However, the limited evidence base to date precludes definitive conclusions regarding the role of breast milk-derived antibodies in modulating vaccine-induced immunity. Nevertheless, the evidence suggests that although maternal antibodies may theoretically reduce vaccine immunogenicity, the overall protective benefits of breastfeeding outweigh any potential interference with vaccine responses.

Background: Pediatric celiac disease (CD) prevalence is rising, estimated at 2% to 3% in select screening cohorts. Affected children face significant environmental, psychosocial, and nutritional barriers within institutional school settings. Methods: This narrative review synthesizes published clinical trials, cohort studies, and food science data to examine infrastructure vulnerabilities and care gaps within educational environments. Results: High-volume school kitchens present potential mechanical cross-contact risks via convection currents and shared equipment. Standard alcohol hand sanitizers demonstrate negligible mechanical or chemical efficacy against inert gliadin proteins, suggesting the need for surfactant-based washing protocols. In classrooms, tactile wheat-based materials introduce non-dietary ingestion pathways. These collective environmental challenges may contribute to social exclusion, peer stigmatization, and heightened risks for childhood mood variations. Furthermore, many commercial gluten-free alternatives lack routine fortification, potentially compounding celiac-related micronutrient deficiencies. Conclusions: Reactive, individualized accommodations may provide insufficient protection. Improving student safety and well-being supported by this narrative evidence points toward a general framework of structured kitchen guidelines, universal classroom adaptations, and jurisdiction-dependent administrative coordination.