The way in which Ebola blocks and disables the body's natural immune response has been revealed in a new study. The understanding of how the virus disarms immune defenses will be crucial in the development of new treatments for the disease.
Researchers at Washington University School of Medicine along with collaborators from the Icahn School of Medicine at Mount Sinai and UT Southwestern Medical Center at Dallas have found how Ebola protein VP24 disrupts the cell's innate immune response, a crucial early step on the virus's path to causing deadly disease.
Gaya Amarasinghe said that they have known for a long time that infection with Ebola obstructs an important immune compound called interferon and now they know how Ebola does this, and that can guide the development of new treatments.
According to the researchers, VP24 works by preventing the transcription factor STAT1, which carries interferon's antiviral message, from entering the nucleus and initiating an immune response. As part of a rapid immune response, the cell allows STAT1 an "emergency access lane" to the nucleus. Rather than block all nuclear transfer, however, VP24 focuses on blocking STAT1's "emergency access lane."
Researchers said that normally interferon causes STAT1 to enter the cell nucleus, where it activates the genes for hundreds of proteins involved in antiviral responses, but when VP24 is attached to STAT1, it can't get into the nucleus.
The study also found that one of the key reasons that Ebola virus is so deadly is because it disrupts the body's immune response to the infection and figuring out how VP24 promotes this disruption will suggest new ways to defeat the virus.
The study was published in the Cell Press journal Cell Host and Microbe.