CEL-SCI Corporation Releases Letter to Shareholders

* Reuters is not responsible for the content in this press release.

Mon Oct 5, 2009 2:30pm EDT

VIENNA, Va., Oct. 5 /PRNewswire-FirstCall/ -- The following letter is being
released by CEL-SCI Corporation (NYSE AMEX: CVM) to its shareholders:


Dear Fellow Shareholders:


After FDA had communicated several weeks ago that we could proceed with our
initial clinical trial with our proposed H1N1 treatment for hospitalized H1N1
patients, we have received many questions with regards to H1N1.  With this in
mind, we have asked one of our outside collaborators, Ken S. Rosenthal, Ph.D.,
Professor, Microbiology, Immunology and Biochemistry, Northeastern Ohio
Universities Colleges of Medicine and Pharmacology, to help explain in
layman's terms the course of the H1N1 disease and why it can be so dangerous. 
Dr. Rosenthal also has provided an explanation of how CEL-SCI's
investigational H1N1 treatment may help in very sick hospitalized patients.
Dr. Rosenthal explains:


Background information on influenza and H1N1 influenza:


Influenza infection could have very mild consequences or cause very severe
disease. At the least, it may seem like a severe cold and at the worst, it can
be life-threatening.  Influenza is a respiratory virus spread in the tiny
water droplets that we release every time we exhale and then are inhaled by
another person.  These droplets enter the mouth and nose and travel down the
throat and into the lungs.  When influenza infects a person's lungs, there are
three destructive components working together to cause disease: the virus's
ability to kill the lung cells; the immune system's inflammatory reactions
that kill influenza infected cells; and bacterial infections that establish
themselves in the diseased environment.   


Influenza virus infects the ciliated epithelial cells of the respiratory tract
that help keep foreign material out of the lungs.  The virus attaches to these
cells through specific sugar molecules, called sialic acids, on the proteins
and lipids on the surface of the cell. Different influenza viruses bind to
variations of these sialic acids.  These sialic acids can be different in
different parts of the lung and so some influenza viruses infect the upper
respiratory tract, like H1N1, whereas others, like avian flu H5N1, infect
cells in the lower lung.  Avian flu also likes the warmer environment that is
deeper in the lung.  While avian flu has high mortality, it is not easily
transmitted because it requires special receptors present on a cell to enter
the cell and  those receptors are only present in cells deep down in the
lungs.  Therefore large amounts of virus are required to infect a patient with
avian flu H5N1.  Swine flu, H1N1, on the other hand, is easily transmitted
because it prefers other receptors to enter a cell and infects the upper
respiratory tract.


After infection, the infected cell becomes a factory to make more viruses. 
Ultimately, when the virus reproduces in the cell, the cell will die.  Before
the cell dies, it sends out a molecular warning to other cells, a cytokine
protein called interferon.  Interferon is an early warning system that puts
other cells on the alert to go on strike and not become a virus factory and
also warns the body to activate immune protections.   The immune protections
cause the flu like symptoms that go with influenza disease.


As the infection progresses and spreads,  white blood cells called dendritic
cells that are in the lung detect the virus, become stimulated and release
other cytokines to activate the body's defenses.  These cytokines include
tumor necrosis factor alpha, interleukin 1 and interleukin 6.  These cytokines
promote inflammation.   Influenza is a very good inducer of these cytokines.
The dendritic cells also activate another white blood cell called a T
lymphocyte, or T cell. The T cell makes even more cytokines that activate
protections, including the production of antibodies by another type of
lymphocyte, called a B cell, as well as killer T cells that travel to the
infection to kill the influenza infected cells.  Although the T cells and
antibody are very important to control and eliminate the virus infection, it
takes a long time (up to about 8 days) before they are ready to do so. By this
time, the virus has spread extensively and caused considerable damage.  Even
though these immune protections are important for controlling the spread of
the virus, they are also very destructive.  Like an ever expanding forest-fire
or a growing war zone, the longer the virus has to reproduce and spread, the
harder it is to control, the more damage it causes and the more damage the
immune response causes to control the infection, peripheral damage to the lung
and surrounding tissue.   


The virus damaged tissue in the respiratory tract is now also more susceptible
to the bacteria that normally reside in the nose, including Staphylococcus
aureus.  The virus kills the ciliated epithelium that pushes these bacteria
out of the lungs and dissolves the mucous lining that protects the underlying
cells.  The infection also exposes cells that are more susceptible to the
bacteria.  As a result, many people who are infected with influenza end up
with a bacterial pneumonia that can be life threatening.


The new H1N1 swine flu virus is a much more lethal virus than previous
influenza viruses, including previous H1N1 influenzas.  Unlike other
influenzas, the new H1N1 virus is especially lethal in young adults.  It
appears that H1N1 may be able to bind to more cells in the lung, reproduce
faster, and spread faster.  The more cells that are infected, the more
difficult it is for the immune system to eliminate the virus and the more
damage the immune system causes by inflammation during the process.  Also,
H1N1 may cause even more cytokines to be produced which also make the
inflammation much more severe.  This is called a cytokine storm.  Young
adults, as they have a very strong immune system, have a very potent
inflammatory response, seemingly more active than in young children or older
adults.  Although it seems illogical, their overactive inflammatory response
may put these individuals at higher risk to serious disease due to the damage
it causes in trying to eliminate the virus infection. 


Influenza vaccines activate immune responses in people that can last for a
long time.  For a vaccinated individual the vaccine induced immune response
can act quickly to stop the reproduction of the virus, limit the spread of the
virus and quickly prevent significant virus damage. Currently there are two
types of influenza vaccines, a live vaccine and a killed vaccine.  A person
receiving the Flumist live vaccine is infected with a weakened mixture of
influenza viruses that cannot cause serious disease but they activate the
immune response to produce T cells that make cytokines to activate T cells 
and other white blood cells that will kill influenza infected cells and
stimulate antibody production.   Other influenza vaccines use inactivated
virus or the H1 and N1 proteins of the virus to immunize a person and produce
only antibodies against the virus.  These vaccines take approximately 10 days
to produce a protective immune response. 


CEL-SCI's DENDRITIC H1N1 TREATMENT


CEL-SCI's dendritic H1N1 treatment, being developed as a treatment for H1N1
hospitalized patients, utilizes the unique LEAPS vaccine technology to convert
an individual's white blood cells into cells targeted to killing influenza. 
The treatment is based on CEL-SCI's L.E.A.P.S. technology.  LEAPS vaccines are
small proteins that combine a piece of an influenza protein with a small
activator protein.  The combined protein activates the dendritic cell, a 
white blood - cell, which presents the influenza protein to the T cell and
then tells that T cell with a focused, controlled amount of cytokine, to grow
and make the cytokines necessary to activate protective T cell immune
responses including killer T cells.  This unique action promotes the
production of inducer cytokines without the tissue damage and flu-symptom
promoting cytokines (pro-inflammatory cytokines), tumor necrosis factor alpha
or interleukin 1.  This helps prevent or get around the issue of cytokine
storm in which the production of too many pro-inflammatory cytokines
contributes to the clinical decline and death of the patient.  The activated
dendritic cells seek out T cells that are specific for H1N1 influenza, present
the influenza protein to them with the appropriate cytokines to get them
excited, increase their numbers so that they can  attack the infected cells
with minimal peripheral damage.  


The dendritic H1N1 treatment customizes the anti- influenza power of the LEAPS
influenza technology.  In short, the dendritic H1N1 treatment causes the
maturation of monocyte white blood cells into dendritic cells that can direct
and activate the subsequent immune response against H1N1 infected cells with
minimal peripheral damage.


End of Dr. Rosenthal's explanation.


We are currently moving forward as fast as is possible with our proposed
dendritic H1N1 treatment for hospitalized H1N1 patients, while proceeding with
due caution and taking all necessary steps to meet regulatory requirements. 
The virus was only discovered 6 months ago and already we are embarking upon
our initial clinical trial.  


With regard to our investigational cancer medicine Multikine, we are preparing
to commence the global Phase III clinical trial designed to support marketing
approval.  The validation of our new manufacturing facility for contract
manufacturing operations is nearing completion, and we have expanded that
validation to cover the manufacturing of Multikine in the new manufacturing
facility as well.  


From my perspective, we are in the best condition ever.  We finally have the
financial resources to move forward on our programs.  Our manufacturing
facility is coming online, the global Phase III cancer trial for Multikine is
being launched together with Teva Pharmaceuticals and Orient EuroPharma as two
of our main partners, and we are racing to develop what we hope to be the
first effective treatment for hospitalized H1N1 patients. We will continue to
keep you up-to-date with any further material developments.   


We thank you for your support as we move forward in several key areas.


Sincerely,
Geert Kersten
Chief Executive Officer


For more information, please visit www.cel-sci.com. 


When used in this report, the words "intends," "believes," "anticipated" and
"expects" and similar expressions are intended to identify forward-looking
statements. Such statements are subject to risks and uncertainties which could
cause actual results to differ materially from those projected. Factors that
could cause or contribute to such differences include, lack of regulatory
clearance to proceed with clinical trials, an inability to duplicate the
clinical results demonstrated in clinical studies that have been completed or
that are initiated in the future, timely development of any potential products
that can be shown to be safe and effective, unwillingness of regulatory
authorities to engage in further regulatory dialogue, receiving necessary
regulatory approvals, difficulties in manufacturing any of the Company's
potential products, inability to raise the necessary capital, and the risk
factors set forth from time to time in CEL-SCI Corporation's SEC filings,
including but not limited to its report on Form 10- K/A for the year ended
September 30, 2008. The Company undertakes no obligation to publicly release
the result of any revision to these forward-looking statements which may be
made to reflect the events or circumstances after the date hereof or to
reflect the occurrence of unanticipated events.


SOURCE  CEL-SCI Corporation

Gavin de Windt of CEL-SCI Corporation, +1-703-506-9460
Comments (0)
This discussion is now closed. We welcome comments on our articles for a limited period after their publication.