If, arginine consumption would cause noticeable herpes activity,
it will imply that the arginine can be used by the asymptomatic
herpes viruses, in order to for them to multiply and grow.

I don't see, how the arginine can be elsewhere used by the viruses,
provided that the neurons, don't "absorb" (or "use" if you wish)
arginine in their constitution.

So, we can conclude, perhaps, some viruses will shed at all times,
right?

P.S.
I've wrote this message , but I did not adequately analysed it; I just
wanted to
post the below, Tim's message, in a related context, before I forget
about it.

Perl Molson

http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&newwindow=1&c2coff=1&safe=off
&selm=Pine.SOL.3.96.1010627133746.21040B-100000%40libra.cus.cam.ac.uk&rnum=5
On 25 Jun 2001, dedale wrote:

Oh ask me an easy one why not :)....oh boy...this might take a while.

Define dormant is the biggest problem, from a clinical perspective,
from
an organism one or from a biochemical one?

From a clinical perspective it certainly is dormant as you get periods
of
disease and disease free state. Asymptomatic shedding also follows
that
pattern with it not being detectable for long periods of time in many
people. However I assume this is not the level you are asking about.

Its the last two perspecitves that complicate matters. Your herpes
infection is not a single entity acting as a whole, its a collection
of individual particles all acting under their own biochemistry. WHen
discussing latency and dormancy us sciencey people are talking about
biochemistry and specifically about the life cycle of individual
viruses.
The conditions one virus particle in one area of the body experience
may
differ to another.

There is a continuum of where between the two extremes of activity,
totally latent and persistently active, any infection in one host is
dependant upon the species of virus. For instance in Epstein Barr
virus
there is commonly some of the virus active in the body at any time and
so
the host is often persistently shedding virus, yet the virus life
cycle
for one copy of a virus does go through the active and latent cycle.
With
VZV that causes chickenpos and shingles you are at the other extreme
the
thing is deeply buried and fidning active virus is so far as I know
virtually impoosible. HSV is osmewhere between the two.

Now to the biochemistry. THe classical view before we had all our
molecular tools was that the virus simply was a circle of DNA that sat
in
its comfortable cell home in the body and under the right conditions
replicated. This view is now well outdated. Examination of the life
cycle
is the hot topic at the moment since it probably holds the key to
controlling the chronic infection of these viruses. It is not fully
understood and there are big gaps in the knowledge of how and when its
working.
Biochemically again there is a spectrum of activity. HSV while latent
produces a single transcript of a restricted portion of its genetic
code.
THis LAT (latency associated transcript) is produced exclusively
during
latency and so far as we know helps maintain it.....when the virus
comes
out of latency a series of different sections of the virus genetic
code
are produced in a specific order leading to activity fo the virus and
production of virus particles. What controls this is unknown, although
there are some indiciations of some of the things that might mediate
it.
Looking at EBV not only do we have nucleic acid code being produced
its
actually then translated into a protein (this hasnt yet been seen in
HSV
despite looking). So the idea f a piece of DNA sitting waiting for a
signal is not an accurate picture of latency, its obviously a dynamic
balance of some kind, under regulation and an active process.

So to try and answer this. THe virus is being periodically active, the
maintainance antibody directly supports this. Triggers can quite
happily
produce an outbreak presumably kicking some latent virus into
activity.
Equally its quite clear that virus can be held, or trather holds
itself
actively in a dormant state at the level of each individual virus
particle. EBV's behaviour equally clearly shows that some virus can
happily be active in latent herpesvirus infections (under the
reasonable
assumption that these viruses share common control systems) while
other
virus in the body is quite.

Whether this means that there is always a cell somewhere in the body
producing virus that kncoked down is essentially unknown and with
current
technology I can see no way of testing it. Whether virus can randomly
attempt to come out equally is unknown just by a random interaction
and if
it gets lucky produce an outbreak or a shedding on top of the
triggered
activities is equally unknown (a kind of random punctuated but
continuous
reactivation idea) or whether control is strong enough that all events
of
virus activation are controlled triggers yet it only takes minor
events to
trigger things is also unknown.

Asymptomatic shedding and the dynamic state that latency actually is
clearly indicate that virus outbreaks are not the end of the story,
and
the true answer could be any of the above ideas, a mixture of them or
something totally different. And it will depend on if you are talking
a
a single virus copy's lifecycle or the body as a whole.

Personally I lean towards a puncuated virus activity cycle in the body
over a continuous one, and I assume there are a number of these that
simply hit the immune system and do nothing more beyond chuck a bit of
virus out of a cell somewhere. Whether its random or direct I simly
cannot
say, and that leaning is esssentially no more than an educated guess,
a
bit like throwing a penny off the Empire State Building, I can tell
you
its gonna hit bottom and it might hit a pedestrian or a paving stone
or a
an auto in the street, but I cant tell you very much more than that.

Tim