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- 12 December 2013 1:00 pm , Vol. 342 , #6164
- About Us
Genetic Variations May Enhance Anthrax Susceptibility
1 October 2001 7:00 pm
After the devastating terrorism of 11 September, the threat of a biological attack has taken on new urgency. One of the most potent biological weapons is the bacterium anthrax, which can be released as deadly spores into the air. Now, scientists seeking to unravel how anthrax kills have discovered it may hijack a protein that shuttles molecules around inside the cell.
Bacillus anthracis primarily infects livestock such as sheep and cattle, although it can kill humans who eat infected animals or inhale the spores. Once in the bloodstream, the bacteria produce so-called lethal toxin (LeTx), which destroys immune cells called macrophages. Macrophages protect the body from harmful bacteria by digesting and destroying them with corrosive chemicals. But LeTx thwarts that system by sneaking inside the macrophages, bursting them open, and releasing deadly toxins.
To better understand how anthrax targets macrophages, geneticist William Dietrich of Harvard University and his colleagues at Harvard and the Whitehead Institute in Cambridge, Massachusetts, searched for a gene they thought might be responsible. The scientists knew that somewhere on chromosome 11 a gene was making certain mice more sensitive than others to anthrax. When the team members compared these mice, they report in the 2 October issue of Current Biology, they found that the resistant mice were protected by a mutated version of a gene for a poorly understood protein called Kif1C.
Kif1C operates inside the cell like a freight train, carrying cargo along molecular tracks called microtubules. No one knows what Kif1C normally transports or how the mutated version may thwart anthrax infection. Dietrich's team expected that functional Kif1C was necessary for anthrax toxin to kill the macrophages; therefore, using a drug to disable Kif1C should make the macrophages resistant to anthrax and might lead to a new treatment. Instead, the opposite was true: Inhibiting Kif1C with a drug called brefeldin-A made resistant animals more susceptible to anthrax. This hints that variations in the Kif1C gene that disable the protein actually enhance anthrax susceptibility.
"It's very strong work," says microbiologist Phillip Hanna of the University of Michigan, Ann Arbor. Hanna says more research will be required to determine how the Kif1c protein contributes to cell death. "Is it the train itself that's being affected ... or is the toxin being delivered to a different site?"