2006/05/01 by Mounira K. Chelbi‐Alix, Aurore Vidy, Jamila El Bougrini +1 · 1 citation
Immunology and Microbiology · Medicine · #interferon and immune responses #Viral Infections and Vectors #Herpesvirus Infections and Treatments #STAT1 #Interferon #Biology #Promyelocytic leukemia protein #Virology #Nuclear transport #Viral replication #Phosphorylation #Interferon regulatory factors #Antiviral protein #Nuclear protein #Gene #Cell biology #RNA #Transcription factor #Virus #Cytoplasm #Cell nucleus #Genetics
paper · doi:10.1089/jir.2006.26.271
openalex publication_date 2006/05/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/22
Interferons (IFNs) are a family of secreted proteins with antiviral, antiproliferative, and immunomodulatory activities. The different biologic actions of IFN are believed to be mediated by the products of specifically IFN-stimulated genes (ISG) in the target cells. The IFN response is the first line of defense against viral infections. Viruses, which require the cellular machinery for their replication, have evolved different ways to counteract the action of IFN by inhibiting IFN production or Jak-Stat signaling or by altering ISG products. This review focuses on the role of viral proteins from the RNA virus family, particularly rabies P protein. P protein mediates inhibition of the IFN system by different pathways: it inhibits IFN production by impairing IFN regulatory factor-3 (IRF-3) phosphorylation and IFN signaling by blocking nuclear transport of Stat1 and alters promyelocytic leukemia (PML) nuclear bodies by retaining PML in the cytoplasm.