Respiratory syncytial virus (RSV) is a pneumovirus of the Paramyxoviridae family of viruses. It is an enveloped virus with a single-stranded, non-segmented, and negative sense RNA genome. RSV remains a major clinical challenge for two reasons:
1. It is highly infectious and thus highly prevalent. Two-thirds of infants are seropositive by their first birthday, and nearly all have been infected by their second birthday. Despite this, reinfection is quite common throughout life; even with a highly similar virus strain, which raises questions about the efficacy of the innate and adaptive immune response to RSV.
2. It is a leading cause of lower respiratory tract disease in infants and young children. RSV bronchiolitis is reported as the leading cause of hospitalization for infants less than 12 months of age and kills more infants than influenza. There is also growing evidence that RSV infection and bronchiolitis increase the risk of asthma and allergy later in life. RSV infection impairs cilia function and infant bronchioles have a more restricted airway resistance, resulting in greater difficulty dealing with the necrotic debris and mucous brought on by an RSV infection of the lower respiratory tract. Moreover, the immune response to RSV in bronchiolitic infants is Th2-biased which promotes smooth muscle contraction and hypersensitivity. These abnormalities lead to a reduction in pulmonary function that can persist for over 10 years.
Despite extensive basic and clinical research, there is still no effective RSV vaccine. Fundamentally, this is due to a lack of understanding of the anti-viral immune response in infants, and the extraordinary sequence variation that occurs in clinical RSV isolates. In this presentation, I will highlight the viral and immunological obstacles that continue to hamper vaccine development, and discuss the most promising treatments of RSV infection and disease.