From Our 2012 Archives
Vulnerability to Anthrax Varies Widely: Study
Latest Infectious Disease News
MONDAY, Feb. 6 (HealthDay News) -- People's susceptibility to anthrax toxin is determined by their genes and can vary greatly among individuals, a new study says.
Anthrax is an infectious disease widely regarded as a potential bioterrorism weapon.
Stanford University School of Medicine researchers analyzed immune cells from 234 people and found that the cells of three of the people were virtually insensitive to anthrax toxin, while the cells of others were hundreds of times more sensitive than those of other people.
The findings could help lead to new treatments and could also have important implications for U.S. national security, according to a university news release. For example, people known to be more resistant could act as first-line responders in an anthrax bioterrorism attack.
The study appears online Feb. 6 in the journal Proceedings of the National Academy of Sciences.
"This research offers an important proof of principle. They've showed that genetically determined variations in the level of expression of a human protein can influence the susceptibility of host cells to anthrax toxin," Dr. David Relman said in the release.
Relman is a professor of microbiology and immunology and of medicine at Stanford, chair of the Institute of Medicine's Forum on Microbial Threats and a member of the U.S. Department of Health and Human Service's National Science Advisory Board for Biosecurity. He was not involved in the study.
"The findings also provide a possible means for predicting who is likely to become seriously ill after exposure, which could be extremely useful when faced with a large number of exposed people, such as was the case during the 2001 anthrax attacks," Relman said. (A week after the 9/11 attacks, letters carrying anthrax spores were mailed within the United States, killing five people and infecting 17 others.)
"Finally, they could lead to the development of novel treatment strategies, perhaps by blocking the interaction between the toxin and the receptor, or by down-regulating its expression," he added.
-- Robert Preidt
Copyright © 2012 HealthDay. All rights reserved.
SOURCE: Stanford University, news release, Feb. 3, 2012
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