Understanding RSV Pathogenesis and Host Immune Response: Implications for Treatment and Prevention

Respiratory Syncytial Virus (RSV) is a globally prevalent pathogen and a leading cause of acute lower respiratory tract infections (LRTIs), particularly among infants, young children, the elderly, and immunocompromised individuals. Despite decades of research, RSV continues to impose a significant health and economic burden due to the absence of long-lasting immunity, the lack of a broadly effective vaccine, and limited therapeutic options. RSV pathogenesis is complex, involving not only direct viral cytopathic effects but also intricate interactions with the host immune system. The virus has evolved mechanisms to evade innate immunity, particularly by antagonizing interferon responses, which allows for sustained replication and contributes to disease severity. In infants, immature and dysregulated immune responses further complicate clinical outcomes, often leading to immunopathology. Existing treatments such as ribavirin and Palivizumab have limited effectiveness, are costly, and are reserved for specific high-risk populations. This review underscores the importance of understanding RSV’s molecular pathogenesis and host immune interactions to inform the development of effective antivirals, immunomodulatory therapies, and next-generation vaccines. Bridging these gaps through interdisciplinary research is essential to reduce RSV-associated morbidity and mortality worldwide, particularly in low-resource settings.