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 Ebola virus (EBOV) could cause disease in mice by suppressing the the cellular mitochondrial antiviral signaling protein (MAVS) signaling and manipulating the interferon response.’
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.
The scientists already knew MAVS had a key anti-EBOV role, and in
the current study examined it in an animal model for the first time.
Many cell types produce MAVS, but MAVS produced by macrophages were
found to be critical in controlling EBOV infection and to limiting the
organ and tissue damage caused by EBOV.
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.