Innate immune evasion by filoviruses.

Christopher F Basler
Author Information
  1. Christopher F Basler: Icahn School of Medicine at Mount Sinai, Dept. Microbiology, Box 1124, 1 Gustave L. Levy Place, New York, NY 10029, United States. Electronic address: chris.basler@mssm.edu.

Abstract

Ebola viruses and Marburg viruses, members of the filovirus family, cause severe hemorrhagic fever. The ability of these viruses to potently counteract host innate immune responses is thought to be an important component of viral pathogenesis. Several mechanisms of filoviral innate immune evasion have been defined and are reviewed here. These mechanisms include suppression of type I interferon (IFN) production; inhibition of IFN-signaling and mechanisms that either prevent cell stress responses or allow the virus to replicate in the face of such responses. A greater understanding of these innate immune evasion mechanisms may suggest novel therapeutic approaches for these deadly pathogens.

Keywords

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Grants

  1. U19AI109664/NIAID NIH HHS
  2. R01 AI059536/NIAID NIH HHS
  3. R01AI05953/NIAID NIH HHS
  4. U19 AI109945/NIAID NIH HHS
  5. U19AI109945/NIAID NIH HHS
  6. U19 AI109664/NIAID NIH HHS

MeSH Term

Ebolavirus
Host-Pathogen Interactions
Humans
Immune Evasion
Interferon Type I
Marburgvirus
Virus Replication

Chemicals

Interferon Type I

Word Cloud

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