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Blocking cell signaling can stymie viral infections, study shows

probable that drugs will lose their potency," Reinherz explains. For short time intervals, blockade of selective cell function is feasible.

In a study published in 2004, Reinherz and his colleagues found that the smallpox virus formally known as variola initiates this process with a signaling protein called smallpox growth factor (SPGF). SPGF flows from the virus to a "receptor" called erb-B1 on the cell surface; when it binds, the cell is primed to become a factory for the virus.

"This suggested that the process of viral replication could be hindered by short-circuiting the SPGF signaling pathway," Reinherz states. To test the idea, they injected SPGF-blocking antibodies into mice infected with a vaccinia virus (it carries a protein much like SPGF), which causes a lethal pneumonia in mice. As hoped, the animals were protected from developing the disease.

In the new study, investigators tested this approach in laboratory-grown cells and in lab animals infected with a pneumonia virus similar to variola. Instead of using antibodies as the SPGF blockers, they used an experimental cancer drug called CI-1033, which is being developed by Pfizer Corp. as a potential cancer treatment. A search of scientific literature revealed that CI-1033 binds to erb-B1, preventing SPGF from signaling through the cellular receptor, even after landing on it.

When they mixed CI-1033 into monkey kidney cells infected with variola, the spread of virus to other cells was blocked. By administering the drug and another compound in mice exposed to the vaccinia virus, the mice not only lived longer than untreated animals but their lungs were cleared of infection. There were also signs that the treated animals produced a stronger immune attack on the virus than the untreated animals did.

Reinherz notes that although CI-1033 itself is not yet an acceptable smallpox treatment -- due to certain side effects -- it represents the type of drug likely to be succe
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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
1-Feb-2005


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