Subs30

Hi Scott

....."had come across anything more on the herpes virus and lab?"....

Yep:

There was study to demonstrate viral latency in the VG(Vestibular Ganglia)---
called:

Prevalence of HSV-1 LAT in Human Trigeminal,
Geniculate, and Vestibular Ganglia and Its
Implication for Cranial Nerve Syndromes

---it was done by:

1 Department of Neurology, Klinikum Grosshadern, LMU
Munich, Germany
2 Max Planck Institute of Neurobiology, Martinsried, Germany
3 Thermo Hybaid GmbH, Ulm, Germany
4 Department of Neurology, University of Pavia, Italy

about a year ago----

The study summary says:

Herpes simplex virus type 1 (HSV-1) enters sensory
neurons and can remain latent there until reactivation.
During latency restricted HSV-1 gene
expression takes place in the form of latency-associated
transcripts (LAT).

LAT has been demonstrated
to be important not only for latency but also for reactivation,
which may cause cranial nerve disorders.
Tissue sections of the trigeminal ganglia (TG),
geniculate ganglia (GG), and the vestibular ganglia
(VG) from seven subjects were examined for the
presence of LAT using the in situ hybridization technique.
LAT was found on both sides in all TG (100%),
on both sides of five subjects (70%) in the GG, and
in none of the VG. Using a second more sensitive
detection method (RT-PCR), we found LAT in the VG
of seven of ten other persons (70%).


This is the first study to demonstrate viral latency
in the VG, a finding that supports the hypothesis that
vestibular neuritis and Labyrinthitis is caused by HSV-1 reactivation.
The distribution of LAT in the cranial nerve ganglia
indicates that primary infection occurs in the TG and
GG and subsequently spreads along the faciovestibular
anastomosis to the VG.

Outstanding on the 90%---it does go---but---man---what a trip!!!