Plays a major role in antagonizing the type I IFN-mediated antiviral response. Acts cooperatively with NS1 to repress activation and nuclear translocation of host IFN-regulatory factor IRF3. Interacts with the host cytoplasmic sensor of viral nucleic acids DDX58/RIG-I and prevents the interaction with its downstream partner MAVS. Together with NS2, participates in the proteasomal degradation of host STAT2, IRF3, IRF7, TBK1 and DDX58 through a NS-degradasome involving CUL2 and Elongin-C. The degradasome requires an intact mitochondrial MAVS. Induces host SOCS1 expression. Induces activation of NF-kappa-B. Suppresses premature apoptosis by an NF-kappa-B-dependent, interferon-independent mechanism promoting continued viral replication. Monomer (instable). Homomultimer. Heteromultimer with NS1. Interacts with host DDX58 (via N-terminus); this interaction prevents host signaling pathway involved in interferon production. Interacts with host MAP1B/microtubule-associated protein 1B. Most NS2 resides in the mitochondria as a heteromer with NS1. The DNLP motif has IFN suppressive functions like binding to host MAP1B. Belongs to the pneumovirus non-structural protein 2 family.