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Researchers Identify Anthrax Resistance Gene in Mice

While fear of a terrorist biological attack in the U.S. escalates, researchers have made progress in understanding how the anthrax bacterium causes disease. Described in the October issue of the journal Current Biology, the new findings could eventually lead to therapies for the often fatal infection.

William F. Dietrich of the Howard Hughes Medical Institute and his colleagues discovered that mice with certain forms of a gene known as Kif1C are resistant to anthrax. Anthrax launches its attack on the body by first wiping out immune system cells called macrophages. But the different forms of the transportation protein made by the resistant Kif1C gene variants appear to protect the macrophages, perhaps by sequestering the toxin in a region of the cell where it can be eliminated. Although the subtle mutations in the resistant variants probably don't affect the macrophages in their normal functioning, Dietrich notes, in the presence of anthrax toxin their effects "can mean the difference between death and survival of the macrophage."

Several of the team's experiments made the effects of the resistant Kif1C variants, or alleles, especially clear. Inserting a resistant allele into susceptible macrophages made the cells more resistant to anthrax. In contrast, when the researchers treated resistant macrophages with a drug known to prevent the Kif1C protein from reaching its target destination, the cells yielded to the toxin. "Research by other groups has indicated that anthrax toxin kills macrophages by inducing a runaway reaction called an oxidative burst," Dietrich remarks. "We speculate that [the Kif1C protein] might be transporting either the elements that are part of this oxidative burst, or the actual oxidative compounds themselves. Or the protein may be ensuring the prompt and appropriate delivery of compounds that protect the macrophage against its own oxidative burst."

Kif1C is known to exist and vary in humans. But whether any of these human variants confer comparable anthrax resistance remains to be seen. "We intend to look for these variations in human populations, to figure out what cargo this protein is carrying, and to learn why Kif1C is activated under anthrax intoxication," Dietrich asserts. "Once we understand such phenomena, we might be able to work toward clinical applications in terms of better diagnostics and treatments."

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