The immunopathology of respiratory syncytial virus (RSV) infection, the
most common cause of lower respiratory tract infections (LRTI) in the
pediatric population, with severe disease being the exception. The
variability of the clinical presentation is incompletely explained by
host, viral and environmental factors but, in infants and young
children, disease severity is certainly linked to the physiological
immune immaturity. There is evidence that the maturation of the host
immune response is, at least in part, promoted by the composition of the
nasopharyngeal microbiome that, modulating excessive inflammation, can
counteract the predisposition to develop viral respiratory infections
and lower the risk of disease severity. However, interaction between the
nasopharyngeal microbiota and respiratory viruses can be bidirectional.
Microbial dysbiosis can drive disease pathogenesis but may also
represents a reflection of the disease-induced alterations of the local
milieu. Moreover, viruses like RSV, can also increase the virulence of
potential pathogens in nasopharynx, which is a main reservoir of
bacteria, and therefore promote their spread to the lower airways
causing superinfection. Negative changes in microbial community
composition in early life may constitute a heightened risk towards
severe RSV respiratory infection and bacterial superinfection, whilst
specific groups of microorganisms can be associated with protection. A
better understanding into the potential negative and positive role of
the different nasopharyngeal bacterial species in disease prevention as
well as into the possible benefits of microbiome therapeutic
manipulation, may improve patient outcomes.
G Protein Variation in Respiratory Syncytial Virus Group A Does Not Correlate with Clinical Severity
