Bronchiolitis needs a revisit: Distinguishing between virus entities and their treatments

Jartti, Tuomas; Smits, Hermelijn H.; Bønnelykke, Klaus; Bircan, Ozlem; Elenius, Varpu; Konradsen, Jon R.; Maggina, Paraskevi; Makrinioti, Heidi; Stokholm, Jakob; Hedlin, Gunilla; Papadopoulos, Nikolaos; Ruszczynski, Marek; Ryczaj, Klaudia; Schaub, Bianca; Schwarze, Jürgen; Skevaki, Chrysanthi; Stenberg-Hammar, Katarina; Feleszko, Wojciech

Typically, as a result of innate immune activation, an early burst of type I/III interferons will occur rapidly after respiratory viral infection. This will be followed by an induction of cytokines, including alarmins, chemokines, and growth factors that activate and attract innate lymphoid cells, granulocytes, dendritic cells, and monocytes to the site of infection. 1, 41, 42 The combined effect of the virus and the inflammatory response leads to epithelial cell apoptosis, necrosis, and epithelial sloughing, as well as mucus overproduction. However, while RSV infections can lead to severe lower respiratory tract infection primarily in very young children, RV infections tend to result in severe wheezing in slightly older children, those with atopic predisposition in particular. 1 In order to understand these differences, we need a better insight into the immunological events in the lungs in as a response to these early respiratory infections. 42,43