Abstract
Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in children <2 years of age. Increased morbidity and mortality have been reported in high-risk patients, such as premature infants, patients with cardiac disease, and severely immune compromised patients. Severe disease is associated with the virulence of the virus as well as host factors specifically including the innate immune response. The role of type I interferons (IFNs) in the response to RSV infection is important in regulating the rate of virus clearance and in directing the character of the immune response, which is normally associated with protection and less severe disease. Two RSV non-structural proteins, NS1 and NS2, as well as the envelope G glycoprotein are known to suppress type I IFN production and a robust type I IFN response to RSV does not occur in human infants or neonatal mouse models of RSV infection. Additionally, presence of type I IFNs are associated with mild symptoms in infants and administration of IFN-α prior to infection of neonatal mice with RSV reduces immunopathology. This evidence has driven RSV prophylaxis and therapeutic efforts to consider strategies for enhancing type I IFN production.
Highlights
Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract disease in infants and young children [1,2,3]
The importance of elucidating the host response to RSV infection is underscored by recent clinical evaluation of prophylaxis with the anti-F protein monoclonal antibody palivizumab in healthy preterm infants
Human IFNs are classified as type I (IFN-I), type II (IFNII), or type III (IFN-III) with each class binding to specific receptors
Summary
Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract disease in infants and young children [1,2,3]. Mice developed good antibody responses despite the attenuated infection [54] These findings suggest that RSV surface proteins signal through multiple pathways, and this may be an important means of reducing anti-viral type I IFN expression, thereby promoting virus replication. The importance of elucidating the host response to RSV infection is underscored by recent clinical evaluation of prophylaxis with the anti-F protein monoclonal antibody (mAb) palivizumab in healthy preterm infants In this singleblind, randomized, placebo-controlled trial, suppression of RSV replication did not have a major effect on reducing the RSVassociated asthma incidence at age 6 years, suggesting that other factors besides viral load contribute to the clinical severity [11, 65]. We review the mechanism surrounding RSV and type I IFN production in humans and mouse models and discuss its implications for development of therapeutics and vaccines
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