Abstract
The epidemiological burden of herpesvirus-induced CNS pathology in children remains substantial despite advances in antiviral therapeutics and vaccination strategies. Current estimates suggest that herpesvirus infections account for approximately 20-30% of all viral encephalitis cases in pediatric patients, with HSV encephalitis carrying mortality rates of 20-30% without prompt treatment and neurological sequelae in up to 70% of survivors. Congenital CMV infection, affecting approximately 0.5-2% of all newborns worldwide, represents a leading cause of non-hereditary sensorineural hearing loss and neurodevelopmental disabilities. The pathogenesis of herpesvirus-mediated neurological damage involves complex interactions between viral virulence factors, host immune responses, and genetic susceptibility determinants. These viruses employ sophisticated mechanisms to breach the blood-brain barrier, evade immune surveillance, and disrupt neuronal function through both direct cytopathic effects and inflammatory-mediated injury. Recent evidence suggests that aberrant immune responses—characterized by dysregulated cytokine production, impaired cellular immunity, and neuroinflammation—play a pivotal role in determining disease severity and long-term neurological outcomes.
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