Respiratory syncytial virus (RSV), also known as human respiratory cell fusion virus (HRSV) and human orthopneumovirus, is a virus that causes respiratory infections in which infected mucosal cells fuse to form a syncytium (Schweitzer and Justice 2020). It is the leading cause of lower respiratory tract infections and hospital visits in infancy and childhood (Read and Bosco 2020). RSV infection results in bronchiolitis, which is classically caused by activated macrophages and eventually resolved by alternatively activated macrophages (Shirey et al. 2010). The promotion of these two alternative macrophage fates appears to be related to RSV-induced COX-2 and LXA4 and RvE1-mediated protective measures (Fig. 4) (Richardson et al. 2005; Shirey et al. 2014). Also, although it does not directly act on the virus, RvD1 inhibits inflammatory signal transduction by polyinosinic-polycytidylic acid, an analogue of RNAs derived from respiratory viruses such as RSV, and the action of RvD1 is mediated by FPR2/ALX and GPR32 (Hsiao et al. 2014). These reports suggest the critical role of SPMs and lipid mediator class shift in the host’s response to RSV in the initial control and final infection clearance.