Respiratory syncytial virus transcription antitermination protein M2-1 (M2-1)

The Respiratory Syncytial Virus (RSV) transcription antitermination protein, commonly known as M2-1, is an essential component of the viral RNA-dependent RNA polymerase (RdRp) complex (UniProt: P04545). Its primary biological function is to act as a processivity factor that prevents the premature termination of viral mRNA transcription at gene-end signals, thereby ensuring the synthesis of full-length viral transcripts (PubMed: 22491456). M2-1 is a zinc-binding protein that functions by interacting with both the viral phosphoprotein (P) and the nascent RNA, a mechanism that is critical for the virus to transition from transcription to replication (PubMed: 23468493). In the context of disease, M2-1 is vital for the replication of RSV, which is a major cause of severe lower respiratory tract infections, including bronchiolitis and pneumonia, particularly in infants, the immunocompromised, and the elderly (PubMed: 30209173). Because M2-1 is highly conserved among RSV strains and has no known human homolog, it is considered a promising target for the development of novel antiviral therapies. Current drug discovery efforts focus on small molecules that can disrupt the M2-1/P protein-protein interaction or interfere with the protein's RNA-binding capacity to inhibit viral load (PubMed: 25589640).

Other names

M2-1 proteinTranscription antitermination factor M2-1RSV M2-1Protein M2-1M2-1

Inhibition of the interaction between M2-1 and the viral phosphoprotein (P) or inhibition of RNA binding.