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Secret to Listeria's virulence provides clues to workings of other deadly intracellular pathogens, UC Berkeley scientists report

Many deadly microbes have learned that the key to launching an infection is not to kill your host - at least not too quickly.

Now, scientists at the University of California, Berkeley, have discovered how one microbe, Listeria monocytogenes, is able to manage this.

In a paper in this week's issue of Science, Daniel A. Portnoy, professor of molecular and cell biology in the campus's College of Letters & Science and professor of infectious diseases in the School of Public Health, along with post-doctoral fellow Amy L. Decatur, describe the trick these bacteria use to live comfortably inside a cell until they're ready to break out and spread the infection to other cells.

The finding could have implications beyond this one bacteria, which causes a deadly disease called listeriosis. The world's top three infectious killers - AIDS, tuberculosis and malaria - all are caused by pathogens that ensconce themselves snugly inside cells and live to wreak havoc. Yet, these intracellular pathogens have been hard to study, Portnoy said.

"There are no effective vaccines for any of these diseases, in part because it is difficult to study intracellular pathogens," he said. "Listeria is a great model system for studying the host-pathogen interaction of these intracellular bugs."

Listeria is a common but deadly bacterium that in recent years has made headlines as a contaminant of hot dogs, cheese, cole slaw and other food stuffs, causing more than two thousand infections every year and 500 deaths. Though it hits immune-compromised people the hardest, its overall fatality rate is about 20 percent.

Listeria bacteria establish an infection by inducing immune system cells, mostly scavenger cells called phagocytes, to corral and swallow them, so that they end up encased in a bubble within the body of the cell. The bacteria would be benign if they remained isolated in the vacuole, because the cell can kill them there. But they eventually break out and take over the
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Contact: Robert Sanders
rls@pa.urel.berkeley.edu
510-643-6998
University of California - Berkeley
1-Nov-2000


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