DENVER - Tuberculosis is a crafty foe. About 2 billion people are infected worldwide, but most show no symptoms, remaining disease-free for life. However in 10 percent of these latently infected persons, weakening of the immune system, caused by either illness or age, allows the tuberculosis bacteria to emerge from small lesions in the lung. The resulting coughing and hacking, which can be fatal if untreated, spreads the bacteria to the next generation of unsuspecting hosts.

Until recently no one knew exactly how the tuberculosis bacteria performed its chameleonlike feat or how to stop it. Now Stanford University Medical Center researchers have begun to understand how Mycobacterium tuberculosis orchestrates its impeccably timed game of hide-and-seek.

"This is an extraordinarily successful survival strategy," said Gary Schoolnik, MD, professor of medicine and of microbiology and immunology at Stanford's School of Medicine. "We're trying to understand how the host's immune system induces and maintains this state of latency." Schoolnik will make his presentation Sunday in Denver at the annual meeting of the American Association for the Advancement of Science in a session called "The Future of Functional Genomics II."

Schoolnik and his colleagues capitalized on the availability of the complete genome sequence of Mycobacterium tuberculosis and the versatility of DNA microarrays to compare the gene-expression profiles of replicating bacteria and bacteria that had been coaxed into latency in the lab. They identified 48 genes involved in the physiological and morphological changes that occur when the bacteria enters its extended hibernation.

"We've discovered a genetic program that contributes to the organism's capacity to persist and which explains, in part, the mechanism for reactivation," said Schoolnik. The secret lies in the ability of the bacteria to respond to a combination of low oxygen levels and increased amounts of nitric oxide -
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Contact: Krista Conger
kristac@stanford.edu
Stanford University Medical Center
16-Feb-2003

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