Anthrax, a bacterial disease that infects livestock and normally poses some risk to humans, is considered one of a number of potential biological weapons. Inhaled anthrax spores kill 90 percent of humans within days of infection.
Presley Professor of Microbiology and Molecular Genetics R. John Collier, who has done research on the proteins that allow anthrax to infect cells, says that he has received about 25 calls from news organizations in the last few weeks.
“It’s certainly much more attention than I’m used to,” he says.
But why has anthrax specifically entered the spotlight?
Dr. Luciana L Borio, a fellow at the Johns Hopkins Center for Civilian Biodefense Studies, says anthrax spores survive well once released and “the size of the spores are perfect for inhalation,” she says. That makes it a perfect weapon for bioterrorists.
And now, the Sept. 11 terrorist attacks have changed the way many people think about the chances of catastrophic terrorism.
“Until now, there’s been no reason why anyone in their right mind would develop a vaccine for plague,” she says. “But that’s all changed.”
Borio says the anthrax baccilus is on the “A” list of diseases capable of causing the most harm if unleashed on a human population.
“I think we’ve always had a threat but the perception has changed,” she says. “People realized that there are not moral limits to what people will do.”
The work of Collier and another Harvard Medical School researcher, Assistant Professor of Genetics William F. Dietrich, focuses on the ways that anthrax enters and destroys cells. Although their research insights are still years away from having clinical benefits for humans, their work has illuminated the molecular aspects of the disease in a way that may eventually be used to fight it.
Collier published a scientific paper in this month’s issue of Nature Biotechnology in which he describes the ability of a protein he discovered to protect rats from anthrax infection. The protein blocks the anthrax toxin’s path into cells.
Working with Mallinckrodt Professor of Chemistry and Chemical Biology George M. Whitesides, Collier bound multiple copies of the protein to a flexible backbone. The connected proteins block the toxin’s entrance into the cell. Separately, Collier has constructed a mutant protein that actually integrates itself into the pore that the toxin enters, blocking its action.
If everything goes well, he says, the mutant protein might yield human therapies in a couple of years.
Borio says the recent attacks are an impetus for research on uncommon but deadly diseases.
She noted that there is no market incentive for companies to develop treatments for many of the diseases that may be used in bioterrorism.
Smallpox, for example. was declared eradicated in 1977. However, stores of the virus are said to exist in both Russia and the U.S., and many people born since the disease was eradicated have not been vaccinated.
One biotechnology company, Cambridge-based Acambis, is under contract with the Centers for Disease Control and Prevention to produce smallpox vaccine. The government has ordered a 40 million dose stockpile. But without the government contract, there would be no reason for a company to produce the vaccine.
In contrast to Collier’s work, which may have applications for vaccines, Dietrich’s work on anthrax focused on genes that cause cells to resist the toxin. In a paper published in this week’s Current Biology, Dietrich describes two alleles, or versions of a gene, that help mice fight off anthrax infections.
If humans have similar genes, they could be used to gauge a person’s risk of death after exposure to the anthrax toxin. But the basic research Dietrich is doing is still far from finding ways to treat the disease.
“In terms of therapy, this has to do with understanding more about the process,”he said.
Dietrich, too, says he is not used to the attention he has been getting.
“It’s surprising to me. Four weeks ago people would not have noticed this paper,” he said.
He said he hopes all the talk about anthrax does not alarm people.
“I don’t want people to be more panicky than they already are,” he said.
—Staff writer Jonathan H. Esensten can be reached at email@example.com.