title: Camouflage and misdirection: the full-on assault of ebola virus disease.
abstract: Ebolaviruses cause a severe hemorrhagic fever syndrome that is rapidly fatal to humans and nonhuman primates. Ebola protein interactions with host cellular proteins disrupt type I and type II interferon responses, RNAi antiviral responses, antigen presentation, T-cell-dependent B cell responses, humoral antibodies, and cell-mediated immunity. This multifaceted approach to evasion and suppression of innate and adaptive immune responses in their target hosts leads to the severe immune dysregulation and "cytokine storm" that is characteristic of fatal ebolavirus infection. Here, we highlight some of the processes by which Ebola interacts with its mammalian hosts to evade antiviral defenses.
authors.affiliation: Boston Children's Hospital, Department of Medicine, Division of Infectious Diseases, Boston, MA 02115, USA.
authors.forename: John
authors.initials: J
authors.lastname: Misasi
authors.affiliation: Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: njsull@mail.nih.gov.
authors.forename: Nancy J
authors.initials: NJ
authors.lastname: Sullivan
mesh_terms: D016207:Cytokines / Q000276:immunology; D029043:Ebolavirus / Q000502:physiology*; D019142:Hemorrhagic Fever, Ebola / Q000276:immunology* / Q000821:virology*; D057131:Immune Evasion; D007108:Immune Tolerance; D056724:Immunity, Humoral; D014764:Viral Proteins / Q000378:metabolism; D053586:Virus Internalization
chemical_list: D016207:Cytokines; D014764:Viral Proteins