Pathobiology of respiratory syncytial virus (RSV)

Respiratory Syncytial Virus (RSV) is the leading cause of lower respiratory tract illness in infants and affects the elderly and the immune-compromised. RSV infection can cause pulmonary obstruction and disease, but the mechanisms contributing to these outcomes remain elusive. Despite the major health burden caused by infection, there is currently no licensed RSV vaccine and treatments are limited. The Special Issue on “Pathobiology of Respiratory Syncytial Virus (RSV)” covers the attributes of disease pathogenesis, immunity, and vaccine development. In an article by Pedro Piedra, “Antibody Response to the Furin Cleavable Twenty-Seven Amino Acid Peptide (p27) of the Fusion Protein in Respiratory Syncytial Virus (RSV) Infected Adult Hematopoietic Cell Transplant (HCT) Recipients” [1], the antibody response in HCT recipients to an immunodominant peptide made by furin cleavage of the F protein, p27, was shown to be detectable in both serum and nasal wash samples; however, 30% of RSV-infected HCT recipients had a substantial decrease in the mucosal anti-p27 antibody. These findings influence current vaccine development efforts.