Respiratory syncytial virus (RSV) is a respiratory tract pathogen that causes significant morbidity and mortality in children aged< 5 years (most disease occurs at age< 1 year) and is a major public health burden worldwide. More than 90% of children are infected at least once with RSV before the age of 2 years [1–3]. RSV accounts for approximately 70% of hospitalizations due to bronchiolitis [1, 4]. In the United States alone, the estimated healthcare costs associated with RSV hospitalizations exceed $950 million, making it a significant economic burden [5]. Further, the RSV burden is disproportionately greater in children aged< 5 years living in developing countries [3]. RSV infection does not confer long-term protection, as reinfections occur throughout life, which poses a significant disease risk in individuals with cardiopulmonary disease, immunocompromised patients, and the elderly [7]. In the elderly, complications of RSV infection often result from exacerbation of underlying pulmonary and cardiac disease.[7].

A member of the Paramyxoviridae family, Pneumovirus genus, RSV exists as an enveloped virus containing a negative-sense, single-stranded RNA genome. The genome encodes for the following 11 proteins: nonstructural proteins (NS1, NS2, and M2-2), the viral nucleocapsid protein (N), phosphoprotein (P), matrix (M), RNA-dependent RNA polymerase (L), M2-1, and 3 surface glycoproteins (G [attachment], F [fusion], and SH [small hydrophobic]). There are 2 RSV major groups, A and B, and multiple genotypes within each group. The protective immune response to RSV