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To the Editors: Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and lower respiratory tract infection in infants, with effects that extend beyond the lungs. Recent reports estimate an encephalitis/encephalopathy rate of 2.2% among hospitalized children with RSV, which may increase to as high as 36.4% among those admitted to the intensive care unit.1,2 Neurologic complications are more frequent in older infants, showing a median age of around 11 months.2 Within this spectrum, seizures represent the predominant manifestation, affecting 85% of the cases, followed by encephalopathy observed in nearly 60%.2 Severe phenotypes such as acute necrotizing encephalopathy, mild encephalopathy with a reversible splenial lesion, acute encephalopathy with biphasic seizures, and late reduced diffusion and acute disseminated encephalomyelitis are rare (<0.1%).2 In isolated reports, manifestations such as ataxia, exotropia, hemiplegia and facial paralysis have also been described.3 Apnea is a clinically relevant manifestation of RSV infection reported in up to 46.6% of cases.1 However, it is generally considered a mixed event, reflecting impairment of brainstem-mediated ventilatory control and inflammation of upper airway vagal pathways, rather than a primary neurological outcome, particularly in infants younger than 6 months and preterm babies.1,4 Notably, in severe RSV disease, hyponatremia-related seizures attributed to syndrome of inappropriate antidiuretic hormone secretion occur in approximately 4% of cases and should be carefully monitored.2 Distinct from the pathophysiology of other respiratory viruses, RSV-associated encephalopathy most commonly corresponds to an excitotoxic subtype, characterized by altered neurotransmission, glutamatergic overactivation and elevated cerebrospinal fluid interleukin (IL)-6 and brain-derived neurotrophic factor levels, both associated with poorer neurologic prognosis.5 Although viral detection in cerebrospinal fluid is uncommon (0.37%), its presence has been associated with long-term neurologic sequelae, suggesting that direct neuroinvasion may coexist.1 Three invasion pathways are described: hematogenous dissemination (“Trojan horse”), direct peripheral nerve infection and olfactory sensory neuron infection.3,4 In murine models, RSV RNA has been identified in the hippocampus and brainstem, producing long-term potentiation deficits in spatial learning and behavioral alterations.3 Maternal infection has also been shown in animal models to cause neurotropic dysregulation associated with autism and behavioral impairments.3 Finally, impaired native-language phonemic learning has also been reported in infants with severe RSV infection before 6 months.4 RSV prevention through maternal immunization and/or monoclonal antibodies is changing the epidemiology and natural history of the disease, particularly in developing countries. Despite being one of the most common pathogens in infancy, few publications have focused on neurologic symptoms and complications, and there are many mysteries unsolved. We urge pediatricians to recognize RSV as a pathogen with genuine neurotropic potential. Growing evidence in animals and humans suggests that RSV may be associated with significant neurological involvement that remains insufficiently documented and may represent an overlooked problem globally. Two priorities emerge (1) standardized definitions of RSV-associated neurologic events, and (2) generation of robust cohorts and evidence in low- and middle-income countries, where the burden of severe RSV disease is highest. Only by integrating these measures, we can truly assess whether current prevention strategies can reduce neurologic involvement and therefore potential sequelae.