Pathogen recognition receptor crosstalk in respiratory syncytial virus sensing: a host and cell type perspective

• Crosstalk of multiple pattern recognition receptors (PRRs) in respiratory syncytial virus (RSV) sensing is cell type-specific.
• RSV entry route and compartmentalization determine PRR ligand accessibility.
• RSV-derived components that bind to PRRs during natural RSV infection remain to be identified.
• Confirmation of PRR function in children is essential for vaccine design.

Human respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in young children, immunocompromised adults, and the elderly. The innate immune response plays a pivotal role in host defense against RSV, but whether severe outcomes following RSV infection result from excessive or poor innate immune recognition remains unclear. Recent research suggests a situation in which crosstalk between families of pattern recognition receptors (PRRs) occurs in a cell type-dependent manner. The current challenge to empower novel therapeutic approaches and vaccine development is to confirm the role of the individual receptors in RSV pathogenesis in humans.