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The Respiratory syncytial virus subtype B (RSV-B) fusion (F) protein is a class I viral fusion glycoprotein essential for the virus's ability to enter host cells [1, 5]. It exists in two primary conformations: a metastable prefusion (PreF) state and a highly stable postfusion (PostF) state [5, 13]. The PreF conformation is the primary target for potent neutralizing antibodies because it displays highly sensitive epitopes, such as site Ø and site V, which are lost during the transition to the PostF state [2, 8]. In the context of disease, the F protein mediates the fusion of the viral envelope with the host cell membrane, leading to respiratory infections that can progress to severe lower respiratory tract disease, bronchiolitis, and pneumonia, particularly in infants and the elderly [11, 13]. Therapeutic strategies targeting the RSV-B PreF protein include stabilized subunit vaccines like Abrysvo, which contains a specific RSV-B PreF component, and monoclonal antibodies like Nirsevimab that bind to the prefusion-specific site Ø to prevent infection [2, 4, 10]. Small molecule inhibitors like Presatovir also target the F protein to lock it in the prefusion state and inhibit viral entry [6].
Neutralization of viral infectivity by blocking membrane fusion and viral entry into host cells.
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