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Biosecurity News in Brief
Study Reveals Possibilities for New Botulism Treatments and CountermeasuresBy Allison Chamberlain, January 12, 2007 A December 21, 2006, study published in the journal Nature reveals new findings on the molecular mechanisms whereby botulinum neurotoxin, the causative agent of botulism, adheres to nerves and disrupts chemical signaling to muscles.[1] As explained in the study, the precise details of this binding process have eluded scientists thus far, so these findings have significant implications for the development of vaccines against this potential bioweapon threat.[1] The research team, comprised of scientists from Stanford University and the Medical School of Hanover in Germany, determined that botulinum neurotoxin serotype B binds to a specific protein receptor of nerve cells, called the synaptotagmin II.[1] According to a January 10, 2007 press release issued by Stanford University, synaptotagmin II is “an important component of synaptic vesicles,” which are tiny sacs that transport the neurotransmitters “from inside the nerve cell to the surface where the neurotransmitters are released.” As described by study author Axel T. Brunger, the “botulinum neurotoxin basically…hijacks synaptotagmin in order to get inside the neuron.”[2] Once inside the neuron, the toxin blocks the release of acetylcholine—a neurotransmitter that is essential to the communication of nerves with muscles.[1] The authors also found that the toxicity of botulinum is greatly affected by even slight alterations in the toxin’s binding residues.[1] For example, as explained in the Stanford press release, changing only one amino acid in the toxin’s molecular structure can significantly reduce its toxicity.[2] Such findings could aid the development of binding inhibitors or other treatments which Brunger sees as “urgently needed, given the concerns about the safety and scarcity of current botulism therapies.”[2] Furthermore, the investigators determined that the binding interactions between botulinum toxin and synaptotagmin II occur with both high affinity and specificity.[1] In light of these findings, the authors conclude that “the basis for the rational development of preventative vaccines or inhibitors against these neurotoxins” has been found.[1] According to the Stanford press release, the potential development of critical bioterrorism countermeasures against botulinum neurotoxin has additional implications for many neuromuscular-related diseases beyond botulism. Research stemming from these findings could lead to treatments for diseases like uncontrolled blinking, lazy eye, and cerebral palsy.[2]
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