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Biotech / Medical : GUMM - Eliminate the Common Cold -- Ignore unavailable to you. Want to Upgrade?

To: caly who wrote (607)	5/19/1999 12:22:00 AM
From: out_of_the_loop	Respond to of 5582

How cold viruses infect humans. In a few sentences, a cold virus binds to the nasal lining cell (called a nasal epithelial cell) by means of a receptor. Binding to a receptor on a cell is like having a key to a door's lock. The door is the cell membrane, the lock is the ICAM and the virus is the key. The receptor to which the viruses bind is called ICAM-1. ** ICAM = Intercellular Adhesion Molecule * Once a virus is in a cell, it borrows the cells' protein-making machinery and replicates many, many copies of itself. Those viral particles are released from the infected cells and continuously infect other neighboring cells and the process repeats itself throughout the life of the infection. The symptoms of the cold are, in general, caused by the inflammatory response that occurs during the time the body is trying to figure out how to make the right antibody to the infecting virus. There are many viruses that cause the common cold. Most are in the rhinovirus family and use this mechanism. Because there are so many and they are different enough from each other so that antibodies formed from other rhinovirus infections are ineffective, vaccines against the common cold are virtually impossible to manufacture. The fact that they share this mechanism of cellualr entry is what makes the simplicity of Zicam so great. How Zicam is made and how it works Zicam is a solution of zinc gluconate in hydroxyethylcellulose. The latter provides the matrix, or "glue", that keeps Zicam attached to the epithelial cells, even if you sneeze much of it out. How it is manufactured is proprietary and I do not know the actual details, but we know it is very inexpensive such that the profit to GUMM is $1.80 a bottle. No fancy machinery or genes or bacteria are involved in its manufacture. It is stable and has a shelf-life much longer than its 1.5 or so years listed on the bottle. Zicam works by blocking the receptors on the cells so that viruses cannot attach and gain entrance. That is why it works. Simply, if you already have a cold, it prevents your re-infection of uninfected cells that was described above. It is this mechanism of BLOCKING the ICAM receptors that is different than that of Tremacamra. Its blockage the receptors is precisely why the makers of Zicam believe it will have a preventive effect and are studying that now. After you see how Tremacamra works, it is easy to understand why Zicam may work better in both therapeutic and preventive modes. How Tremacamra is made and works Tremacamra is a copy of the ICAM receptor itself. Using the lock analogy, Zicam works by plugging the lock so that the key (the virus) cannot work, and Tremacamra works by adding a bunch of locks that the virus can attach to. They dilute the effectiveness of the virus in attaching to the cells because many of the viruses end up binding to the other locks, the manufactured Tremacamra molecules. In a word, Zicam blocks the virus and Tremacamra competes with the virus for its ICAM-binding site. Viruses can still attach to cells. Thus, Zicam has the better mechanism of action. Tremacamra is a biologically genetically engineered protein. Briefly, scientists figure out the structure of a protein, then backfigure out what the building blocks (amino acids) are, then they backfigure out the RNA structure that codes for those amino acids (hundreds and thousands of them), then they backfigure the DNA and/or messenger RNA required to make those amino acid chains. Sounds complicated. It is, but in fairness, it is getting cheaper, but it will never be as cheap as mixing up a solution of zinc gluconate and putting in its patent-pending proprietary nasal gel matrix. So, in review, Tremacamra is a genetically manufactured protein that is a carbon copy of the ICAM-receptor. The nasal spray puts copies of this "decoy" ICAM-receptor into the nasal passsage to try to fool the virus into distraction. Clearly, to be effective, it must outnumber the real receptors. It is a competes rather than blocks the receptor directly, as Zicam does. (to be continued)...