“A key aspect of anthrax spore biology concerns the germination process through which the dormant spore becomes a reproductive, disease-causing bacterium,” explained Al Claiborne, the study’s principal investigator. “The potential importance of such a germination control mechanism in anthrax is clear, as spore germination and outgrowth are fundamental to proliferation.”
Claiborne, co-director of Wake Forest’s Center for Structural Biology, added, “Basic understanding of the regulatory signals that promote germination will enable discoveries leading to drugs that block the process.”
The research is being paid for by a grant from the Southeast Regional Center of Excellence in Biodefense and Emerging Infections, based at Duke University, one of eight such regional centers funded by the National Institute of Allergy and Infectious Diseases.
The other institutions in Claiborne’s project include a co-investigator at Virginia Tech and collaborators at the US Army Medical Research Institute of Infectious Diseases in Maryland, and the University of California in San Diego.
The research stems from lessons learned from studying the bacteria that cause Staphylococcus infections and two other bacteria in the same group as anthrax.
Claiborne said the group proposes that a vitamin B5 derivative known as Coenzyme A plays a crucial role in the germination of the anthrax spores. They have already shown that anthrax is missing a similar cofactor called glutathione that is common to many other bacteria, as well as humans.
The researchers are working with a non-pathogenic strain of anthrax. The genome sequences of four strains of the bacteria, known scientifically as bacillus anthracis, have been determined.