Abstract
Respiratory Syncytial Virus (RSV), primarily recognized as a respiratory pathogen, has emerged as a potential contributor to neurodegenerative diseases via the "lung-brain axis." Preclinical studies highlight RSV-induced energy metabolism dysfunction as a core pathological mechanism encompassing mitochondrial dysfunction, glucose metabolism reprogramming, and microglial metabolic polarization-critical gaps in clinical validation, molecular specificity, and translational relevance. This review addresses these limitations by advocating for enhanced epidemiological research, detailed molecular pathway characterization, and the integration of human-relevant models. Targeted metabolic interventions have been proposed, supported by recent mechanistic insights, to bridge the gap between hypotheses and therapeutic development.