EMBARGOED FOR RELEASE UNTIL 4 PM ET, April 17, 2002
"Cell Death" Mechanism Identified, May Lead to Improved Treatment of Herpes Simplex Encephalitis
Denver, Colo. -
The key to unlocking improved therapies for herpes simplex encephalitis may lie in identifying the specific mechanisms of virus-induced neuronal degeneration that occurs with this disease. A significant step in this discovery process has recently been made by researchers who have identified a link between apoptosis, or "programmed cell death" and herpes simplex encephalitis (HSE), according to a study presented at the 54th Annual Meeting of the American Academy of Neurology. "This is the first demonstration of apoptotic neuronal death in immunocompetent patients with HSE," explains study author Roberta DeBiasi, MD, of the University of Colorado Health Sciences Center in Denver. "These apoptotic, or dying, neurons appeared to be a result of direct viral injury, rather than as a consequence of secondary inflammatory responses." Apoptosis is a particular form of cell death. It doesn''t just happen to a cell, it is actually a program the cell carries out to kill itself, in response to an environmental signal, such as viral infection. "Part of the reason we don''t yet have better treatments for HSE is that we don''t fully understand how the brain cells die," says DeBiasi. "Our study shows that apoptosis is at least one important way that brain cells die in response to HSE viral infection." HSE is the most common severe encephalitis affecting previously normal people in North America. Twenty percent of HSE patients still die with current treatment options; 40 percent of those who survive end up with significant neurological problems. Until recently, research of this nature has been limited largely to the study of immunocompromised patients with HIV-related neurologic disease. This study examined ten immunocompetent patients with herpes simplex encephalitis (HSE). The presence of apoptotic cells in HSE was correlated with active infection and occurred in the same distribution as tissue injury. Apoptotic cells were also found in additional patients with acute congenital cytomegalovirus encephalitis and PML (progressive multifocal leukoencephalopathy) due to JC virus infection. "We hope that our findings are an important step toward developing improved therapeutic strategies for this devastating disease," concludes DeBiasi. Further study may articulate the complicated series of events between when viral infection occurs and when the cell actually kills itself. "Our lab is working hard to discover the specific pathways by which apoptosis occurs in virus-infected neurons, and to identify which pathways might serve as promising drug targets." The study was made possible with the support of the Department of Veterans Affairs, the U.S. Army, the National Institutes of Health, and an Ortho-McNeil Young Investigator Award.