Abstract
Human respiratory syncytial virus (RSV) is a common and highly contagious viral agent responsible for acute lower respiratory infection in infants. This pathology characterized by mucus hypersecretion and a disturbed T cell immune response is one of the major causes of infant hospitalization for severe bronchiolitis. Although different risk factors are associated with acute RSV bronchiolitis, the immunological factors contributing to the susceptibility of RSV infection in infants are not clearly elucidated. Epidemiological studies have established that the age at initial infection plays a central role in the severity of the disease. Thus, neonatal susceptibility is intrinsically linked to the immunological characteristics of the young pulmonary mucosa. Early life is a critical period for the lung development with the first expositions to external environmental stimuli and microbiota colonization. Furthermore, neonates display a lung immune system that profoundly differs to those from adults, with the predominance of type 2 immune cells. In this review, we discuss the latest information about the lung immune environment in the early period of life at a steady state and upon RSV infection and how we can modulate neonatal susceptibility to RSV infection.
Highlights
Human respiratory syncytial virus (RSV) was isolated for the first time in chimpanzees and identified in 1957 in children with severe lower respiratory illness [1,2,3]
High levels of anti-inflammatory type 2 T helper cell (TH2) cytokines, such as interleukin-4 (IL-4), IL-13, and IL-15, have been detected in mice vaccinated with formaldehydeinactivated RSV vaccine (FIRSV) [11, 12]
We describe the first innate responses of pulmonary resident cells to RSV infection that contribute to the development and/or maintenance of anti-RSV TH2 immunity (Figure 2)
Summary
Human respiratory syncytial virus (RSV) was isolated for the first time in chimpanzees and identified in 1957 in children with severe lower respiratory illness [1,2,3]. High levels of anti-inflammatory type 2 T helper cell (TH2) cytokines, such as interleukin-4 (IL-4), IL-13, and IL-15, have been detected in mice vaccinated with FIRSV [11, 12] This dramatic episode highlights the need to improve our knowledge of infant immune responses to viral infection as well as of RSV pathogenesis in newborn airways. Thereby, as in human infants, the age of neonatal mice at initial RSV infection determines the clinical outcome upon RSV reexposure at adult age These data suggest that RSV infection during the neonatal period is responsible for an immunopathological imprinting in the lungs that could influence the development and the severity of disease and long-term respiratory disorders. We discuss different approaches to modulate the young susceptibility to RSV infection by targeting the neonatal window of intervention
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