Abstract • 66

Respiratory syncytial virus (RSV) is the most common respiratory pathogen to infect children, and RSV lower respiratory tract infection (LRTI) in infants has been linked to childhood respiratory sequelae that present clinically as asthma or reactive airways disease. This relationship has been recognized in the majority of case-control and prospective studies during short-term follow-up of both previously healthy and high-risk infants with RSV LRTI. Several mechanisms explain how RSV LRTI results in respiratory sequelae. These include increased airways inflammation resulting from the effects of RSV infection on the immune responses, enhanced synthesis of inflammatory mediators, and increased production of immunoglobulin E antibodies. Recent investigations have suggested that infection with RSV initiates a release of soluble mediators from a variety of respiratory tract cells. These result in recruitment of other cellular elements to respiratory mucosa, which in turn release other cytokines. The nature of cytokine cascade ultimately influences IgE and IgA antibody responses, and expression of cell surface receptors necessary for mobilization of inflammatory cells and lymphocytes to the site of disease. These include MHC Class 1 and Class 2, ICAM-1, VCAM-1 and other adhesion molecules. Thus, the outcome of clinical infection and development of disease following RSV infection is determined by both immunoregulatory and pro-inflammatory responses during cell-virus interaction in the respiratory tract.