2011/09/07 by Parameshwaran Ramanan, Reed S. Shabman, Craig S. Brown +3 · 84 citations
Medicine · #Viral Infections and Outbreaks Research #Viral Infections and Vectors #Viral gastroenteritis research and epidemiology #Innate immune system #Biology #Immune system #Interferon #Filoviridae #Ebolavirus #Virology #Karyopherin #Acquired immune system #Immunology #Cell biology #Ebola virus #Virus #Nuclear transport #Viral disease #Cytoplasm #Cell nucleus
paper · pdf · doi:10.3390/v3091634
published in Viruses 3(9), 1634-1649 (Multidisciplinary Digital Publishing Institute)
openalex publication_date 2011/09/07 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/06
The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render the host incapable of mounting effective innate or adaptive immune responses. The Type I interferon (IFN) response is critical for establishing an antiviral state in the host cell and subsequent activation of the adaptive immune responses. Several filoviral encoded components target Type I IFN responses, and this innate immune suppression is important for viral replication and pathogenesis. For example, EBOV VP35 inhibits the phosphorylation of IRF-3/7 by the TBK-1/IKKε kinases in addition to sequestering viral RNA from detection by RIG-I like receptors. MARV VP40 inhibits STAT1/2 phosphorylation by inhibiting the JAK family kinases. EBOV VP24 inhibits nuclear translocation of activated STAT1 by karyopherin-α. The examples also represent distinct mechanisms utilized by filoviral proteins in order to counter immune responses, which results in limited IFN-α/β production and downstream signaling.