The Ebola virus disease (EVD) is a severe, often fatal illness in humans. A new mouse model of early Ebola virus (EBOV) infection has shown
National Institutes of Health (NIH) scientists and colleagues how early
responses of the immune system can affect development of EBOV disease.
The model could help identify protective immune responses as targets for developing human EBOV therapeutics. Scientists from NIH's National Institute of Allergy and Infectious Diseases led the study with colleagues from the University of Washington and Columbia University.
The scientists analyzed signals that host cells use to alert the immune system to EBOV infection, and the immune system's responses. They focused on signaling events that begin within hours of a virus infection and involve the cellular mitochondrial antiviral signaling protein or MAVS.
In their experiments, macrophages coordinated the development of more advanced immune responses and the production of type I interferon, a compound with potent antiviral activity.
They also learned that EBOV could cause disease in mice by suppressing MAVS signaling and manipulating the interferon response.
With a goal of eventual drug development, the researchers are continuing their work to pinpoint the precise immune responses controlled through MAVS and to learn more about how EBOV sometimes delays immune signaling.