[Note: this article discusses using alpha herpes viruses (herpes simplex
viruses HHV-1 and HHV-2, and varicella zoster - the virus responsible for
chickenpox and shingles - HHV-3, but not any of the herpes viruses I have
seen mentioned in association with ME or CFS: EVB (HHV-4), cytomegalovirus
(HHV-5) or HHV-6 or HHV-7), but as a model organism: that is, something
studied because it's convenient which they think can provide insight about
how things work in similar situations.
That is to say, the researchers think their work could apply broadly to any
infection which is able to affect the nervous system. e.g. any organism
which could be associated with, or produce, ME could theoretically work in
this manner, although they have not studied those here.
Because of copyright law, I have included only a little of the article here
and one will need to follow the link to read it all on ProHealth.
Findings suggest that other neurotropic viruses (e.g., West Nile or
polioviruses) could corrupt mitochondria in the same way.
Note: This news, written by Morgan Kelly, is provided courtesy of the
Princeton University Office of Communications.
To spread, nervous system viruses sabotage cell, hijack transportation
Herpes and other viruses that attack the nervous system may thrive by
disrupting cell function in order to hijack a neuron's internal
transportation network and spread to other cells. [A process that stops
mitochondrial energy generation in the cells.]
Princeton University researchers made the first observation in neurons that
common strains of the herpes virus indirectly take control of a cell's
mitochondria, the mobile organelles that regulate a cell's:
. Energy supply,
. Communication with other cells,
. And self-destruction response to infection.
The team reports in the journal Cell Host and Microbe [May 17,
"Alpha-herpes virus infection disrupts mitochondrial transport in neurons"]
that viral infection elevates neuron activity, as well as the cell's level
of calcium - a key chemical in cell communication - and brings mitochondrial
motion to a halt in the cell's axon, which connects to and allows
communication with other neurons.
The authors propose that the viruses then commandeer the proteins that
mitochondria typically use to move about the cell.
the link to the publishing journal (I have not read the full text; I just
thought it sounded interesting from the ProHealth article):
To vote for the Hunter-Hopkins Center to win an Intuit grant:
http://bit.ly/pgWc2V (ideally, once per session, which is currently once per
The PACE trial announced that status quo was great for ME/CFS, but is this
conclusion appropriate? See an analysis here: