The Ebola virus harms the body’s natural defenses by binding directly to white blood cells, which expedites the virus’ lethal effects, according to a recent study by researchers at the University of Texas Medical Branch at Galveston (UTMB), the University of Washington, and the National Institute of Allergy and Infectious Diseases (NIAID).
The research teams found that when a person is infected with the virus, their white blood cells that help fight infection, called lymphocytes, quickly disappear. The researchers said those who eventually die from the virus often have low levels of those cells, whereas people who ultimately survive typically maintain their lymphocytes levels over the course of the disease.
While the virus cannot infect the white blood cells themselves, the infection still causes those specific cells to die off. Previously, researchers knew that the virus affects cells and pathways that are critical to lymphocyte health. The study found that the when Ebola binds to lymphocytes, the TLR4 pathway activates cells which contribute to lymphocyte death and leaves individuals more vulnerable to viral infection.
“Adding a chemical that blocks TLR4 activation protected the lymphocytes in the presence of Ebola, confirming its role in infection and spread of disease throughout the body,” Mathieu Iampietro, UTMB researcher and co-lead author of the study, said.
Patrick Younan, co-author of the study, said their findings suggested that drugs that block TLR4 could be used to treat patients with Ebola, which extended an earlier finding that the TLR4 receptor antagonist Eritoran protects individuals against both the Ebola and Marburg viruses.
Findings from the study were published in a recent issue of the medical journal PLOS Pathogens.