Filoviral immune evasion mechanisms

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,...

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Bibliographic Details
Published in:Viruses 2011-09, Vol.3 (9), p.1634-1649
Main Authors: Ramanan, Parameshwaran, Shabman, Reed S, Brown, Craig S, Amarasinghe, Gaya K, Basler, Christopher F, Leung, Daisy W
Format: Article
Language:English
Subjects:
Adaptive Immunity
Animals
Ebolavirus
Ebolavirus - immunology
Ebolavirus - metabolism
Ebolavirus - pathogenicity
Filoviridae
Hemorrhagic Fever, Ebola - immunology
Hemorrhagic Fever, Ebola - virology
Humans
IFN antagonist
Immune Evasion - immunology
Immunity, Innate
innate immune evasion
Interferon Type I - metabolism
Marburg Virus Disease - immunology
Marburg Virus Disease - virology
Marburgvirus
Marburgvirus - immunology
Marburgvirus - metabolism
Marburgvirus - pathogenicity
Phosphorylation
Review
Signal Transduction
Viral Proteins - metabolism
Virus Replication
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Summary: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.
ISSN:1999-4915
1999-4915
DOI:10.3390/v3091634