"We have known for a long time that infection with Ebola obstructs an important immune compound called interferon. Now we know how Ebola does this and that can guide the development of new treatments," said Gaya Amarasinghe from Washington University's school of medicine.
The team, along with investigators from the Icahn School of Medicine at Mount Sinai University and University of Texas' Southwestern Medical Center at Dallas, show how the Ebola protein VP24 disrupts the cell's innate immune response - a crucial early step on the virus's path to causing deadly disease.
One of the key reasons that Ebola virus is so deadly is because it disrupts the body's immune response to the infection.
"Figuring out how VP24 promotes this disruption will suggest new ways to defeat the virus," added Chris Basler of the Icahn School of Medicine at Mount Sinai.
According to researchers, VP24 works by preventing the transcription factor STAT1, which carries interferon's antiviral message, from entering the nucleus and initiating an immune response.
The Ebola outbreak in West Africa has brought a lot of attention to the deadly virus.
According to the World Health Organisation (WHO), up to 90 percent of those infected with Ebola die from the virus.
The paper appeared in the journal Cell Host & Microbe.