Respiratory syncytial virus (RSV) is amongst the most important pathogenic infections of childhood and is associated with significant morbidity and mortality. Although there have been extensive studies of epidemiology, clinical manifestations, diagnostic techniques, animal models and the immunobiology of infection, there is not yet a convincing and safe vaccine available. The major histopathologic characteristics of RSV infection are acute bronchiolitis, mucosal and submucosal edema, and luminal occlusion by cellular debris of sloughed epithelial cells mixed with macrophages, strands of fibrin, and some mucin. There is a single RSV serotype with two major antigenic subgroups, A and B. Strains of both subtypes often co-circulate, but usually one subtype predominates. In temperate climates, RSV infections reflect a distinct seasonality with onset in late fall or early winter. It is believed that most children will experience at least one RSV infection by the age of 2 years. There are several key animal models of RSV. These include a model in mice and, more importantly, a bovine model; the latter reflects distinct similarity to the human disease. Importantly, the prevalence of asthma is significantly higher amongst children who are hospitalized with RSV in infancy or early childhood. However, there have been only limited investigations of candidate genes that have the potential to explain this increase in susceptibility. An atopic predisposition appears to predispose to subsequent development of asthma and it is likely that subsequent development of asthma is secondary to the pathogenic inflammatory response involving cytokines, chemokines and their cognate receptors. Numerous approaches to the development of RSV vaccines are being evaluated, as are the use of newer antiviral agents to mitigate disease.

There is also significant attention being placed on the potential impact of co-infection and defining the natural history of RSV. Clearly, more research is required to define the relationships between RSV bronchiolitis, other viral induced inflammatory responses, and asthma.

References：

1, Modulation of host adaptive immunity by hRSV proteins; Virulence. 2014;5(7):740-51. doi: 10.4161/viru.32225.

2, Respiratory syncytial virus entry and how to block it; Nat Rev Microbiol. 2019 Apr;17(4):233-245. doi: 10.1038/s41579-019-0149-x.

3, Palivizumab, a humanized respiratory syncytial virus monoclonal antibody, reduces hospitalization from respiratory syncytial virus infection in high-risk infants. The IMpact-RSV Study Group;Pediatrics. 1998 Sep;102(3 Pt 1):531-7.

4, Antibody development for preventing the human respiratory syncytial virus pathology;Mol Med. 2020 Apr 17;26(1):35. doi: 10.1186/s10020-020-00162-6.

5, Product review on the monoclonal antibody palivizumab for prevention of respiratory syncytial virus infection; Hum Vaccin Immunother. 2017 Sep 2;13(9):2138-2149. doi: 10.1080/21645515.2017.1337614. Epub 2017 Jun 12.

6, A proof of concept for structure-based vaccine design targeting RSV in humans; Science. 2019 Aug 2;365(6452):505-509. doi: 10.1126/science.aav9033. 7, Respiratory syncytial virus--a comprehensive review; Clin Rev Allergy Immunol. 2013 Dec;45(3):331-79. doi: 10.1007/s12016-013-8368-9.