Both synthetic ssRNA and ssRNA viral genomes activated IRF-3 in a NOD2- and MAVS-dependent manner, and infection with RSV resulted in increased NOD2 expression, leading to IFN production within 2 h p.i., whereas other PRRs (e.g., RIG-I) activate the IRF-3-IFN pathway during a later infection period. The gene discussed is MAVS; the disease is infection.