No; where you see in here any mentions about toothbrushes?

It is probably need of only a few viruses out of many that will
reach a toothbrush, to cause
an infection.

The environment of the toothbrushes can offer lots of
hiding places for those viruses.

But that's really not what I am focusing my attention right now.
I have other unanwered questions such as,
what is the role of the outside the ganglia situated viruses,
in relationship with the traces of the viruses found in ganglia,
in order for them traces of viruses to become active virions?

My guess is, whether in the absence of any viruses or virions outside
the ganglia, can those traces become active virions?

I know it sounds hard to believe, but it actually might be true.

When first infected, the viruses will reach the ganglia; meanwhile,
some viruses will remain on the OB area; furthermore, due to their
singalling
of some sort, these viruses situated on the OB areas,
will trigger some viruses from the ganglia to become virions and some
of
them will travel to the location in the top of the spinal cord or CNS.
(you can see in here the story, that I am talking about):
http://www-ermm.cbcu.cam.ac.uk/99000381h.htm

From now on, there will be some viruses along the neural axons, (where
they
can form new viruses, too), also some viruses at the location
I've just mentioned, that is the spinal cord of CNS.

My guess is, that for as long as there are viruses there in these 2
locations,
those viruses can keep a constant flow of virions and formations of
new virions in ganglia.

That is why, my pressumtion is that if we can eliminate all those
viruses from the axons, the CNS and of course those
from the assymtomatic shedding areas of the skin/mucosa (which is
quite easy to do, with antiviral creams and other methods), then there
will be left only
some unable fragments, traces to become new virions.

Another explanation would be that, the viruses outside the ganglia,
when travelling towards the ganglia, they can cause a local
immunity weakness and thus, allow new virions to escape the ganglia.

As my theory goes, considering that local immunity that
exists around the ganglia, in immediate vicinity of those fragments
that want to become virions, there would be no
possible way for that immunity to allow new virions to be formed.

Only an outside ganglia viral mechanism of disturbance of ganglia
would be, in my opinion, possible.
On the other hand, those viruses situated outside ganglia, they
can't cause an OB themselves, either; they are only able to
disturb that local immunity near the ganglia and
thus, as I've said, allowing for new virions to be formed in ganglia.

There is this combined mechanism of external from ganglia viruses
that will only contribute to allowing the new ganglia virions to be
formed
(of course, in large numbers, that will be able to overcome the
further
immunity that the viruses need to overcome in order to reach the
skin/mucosa
for an OB; there should be at least 2 different types if not more, of
such immunity that the large number of viruses will require to
overcome).

Let me recap, now, to make a long story short:

In a cronic infected person, there are some viruses
found at the CNS, that is spinal cord, some viruses found inside the
neurons; in both of these situations, the viruses are not
capable of causing independently, an OB.
The way the OB will take place, is, due to the local immunity problem,
that is being caused by the viruses, that will return back to the
ganglia, from
these, at least one location: neuron or CNS.

With the local immunity at the ganglia weaken, now the large number of
new formed viruses will be able to overcome all other immunity meed
until the skin/mucosa.

To be even more clear in my explanation, imagine this scenario
that I've seen in a documentary on tv.

A gang of bank robbers, I recall let call them herpes viruses; there
were a group of prisoners inside a jail. Their friends, free at that
moment,
have helped those jailed men to escape. Thus, together, they'd started
robbing banks and such.

Do you see my point?
That is how I understand HSV, at the moment.

Perl Molson