"If mitochondria are stopped in their tracks and can't go anywhere, that is potentially very bad," he said. "They are not only the power plants of the cell, but regulate important processes. The virus likely acts to interfere with many of those processes."
Beyond herpes, the Princeton findings present a possible explanation for how other neurotropic viruses such as rabies, West Nile and polio attack and disrupt the nervous system, Kramer said. Although these viruses are different from the herpes family, the fact that HSV-1 and PRV had a similar effect on mitochondrial motion and function suggests that other pathogens could corrupt mitochondria in the same way, he said.
In addition, the paper lays out the implications of distorted mitochondrial function on neuron health. Mitochondrial malfunction is a known factor in non-infectious neurodegenerative conditions such as Alzheimer's disease and Parkinson's disease, Kramer said, though the pathway to this disruption is not entirely known.
"Our model raises some new and exciting possibilities for future research on other important human viruses that can invade the nervous system and cause disease," Kramer said.
"And the fact that alpha-herpes infection damages the same key cellular function as neurodegenerative disorders also is striking," he said. "Understanding how viral infection damages neurons might give us insight into how diseases like Alzheimer's do the same. The viruses we study hijack well-studied cellular pathways that might make an effective target for future therapeutic strategies."
In a healthy neuron, mitochondria move throughout the cell's elongated, tree-like structure to provide energy for various processe
|Contact: Morgan Kelly|