One of the human body's first responses to a viral infection is to make and release signaling proteins called interferons, which amplify the immune system response to viruses. Over time, many viruses have evolved to undermine interferon's immune-boosting signal, and a paper published today in the journal Cell Host & Microbe describes a mechanism unique to the Ebola virus that defeats attempts by interferon to block viral reproduction in infected cells.
The newly published study explains for the first time how the production by the virus of a protein called Ebola Viral Protein 24 (eVP24) stops the interferon-based signals from ramping up immune defenses. With the body's first response disabled, the virus is free to mass produce itself and trigger the too-large immune response that damages organs and often becomes deadly as part of Ebola virus disease (EVD).
The study was led by scientists from Washington University School of Medicine in St. Louis in collaboration with researchers from the Icahn School of Medicine at Mount Sinai and the University of Texas Southwestern Medical Center.
"Our study is the first to show how Ebola viral protein 24 defeats the signal sent by interferons, the key signaling molecules in the body's early response to Ebola virus infection," said Christopher F. Basler, PhD, Professor of Microbiology at the Icahn School of Medicine at Mount Sinai, and an author of the newly published paper. "These newfound details of Ebola biology are already serving as the foundation of a new drug development effort, albeit in its earliest stages," said Dr. Basler, also a researcher within the Mount Sinai Global Health and Emerging Pathogens Institute.
"We've known for a long time that infection with Ebola virus obstructs an important arm in our immune system that is activated by molecules called interferons," said senior author Gaya Amarasinghe, PhD, Assistant Professor of Pathology and Immunology at Washington U
|Contact: Greg Williams|
The Mount Sinai Hospital / Mount Sinai School of Medicine