Previous research has shown that HSV-1 and PRV also use kinesin-1 specifically for transport within an infected cell. Thus, Kramer said, his and Enquist's work suggests that it is very likely that the viruses disrupt mitochondrial motility so that they can hitch themselves to the now available kinesin-1 proteins and move through the nervous system more efficiently.
James Alwine, a University of Pennsylvania professor of cancer biology, said that the Princeton research is a significant contribution to a growing body of research that describes how viruses seize cellular motor proteins such as kinesin-1.
While the findings have therapeutic potential particularly in helping show how balancing cellular calcium might subdue viral infection the demonstration that viruses can move through an infected cell with the ease of something as essential as mitochondria is notable in itself, said Alwine, who is familiar with the research but had no role in it.
"Determining the specific mechanism by which Miro function is abrogated may provide additional therapeutic avenues, but this also is marvelous basic research that does not have to be justified by its therapeutic potential," he said.
"To disrupt the loading of mitochondria to motor proteins so that virions [complete virus particles] can load instead is a clever way for a virus to be transported and is a great new idea provoked by this data," Alwine said. "While other neurotropic viruses would have to be tested specifically, movement in nerve cells is required by all of them. Thus, this observation provides a starting place and a model mechanism for research with those other pathogens."
|Contact: Morgan Kelly|