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Fungal infections can be devastating to human health, killing approximately 150 people every hour, resulting in more than 1 million deaths every year, more than malaria and tuberculosis combined. Unfortunately the antifungal drug arsenal is limited, with many of the best drugs more than 50 years old. The search for new antifungals has recently alighted on a simple biological pathway, the production of trehalose, a chemical cousin to table sugar that pathogenic fungi need to survive in their human hosts. A team of Duke researchers has solved the structure of an enzyme that is required to synthesize this fungal factor.

When new AIDS virus particles bud from an infected cell, an enzyme named protease activates to help the viruses mature and infect more cells. That's why modern AIDS drugs control the disease by inhibiting protease. Now, University of Utah researchers found a way to turn protease into a double-edged sword: They showed that if they delay the budding of new HIV particles, protease itself will destroy the virus instead of helping it spread. They say that might lead, in about a decade, to new kinds of AIDS drugs with fewer side effects.