DENVER, CO -- 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 April 17 at the 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, M.D., 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 doesnt 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 dont yet have better treatments for HSE is that we dont 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.