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If you were a pathogen under attack from the immune system—say, a food-borne Salmonella or Listeria bacterium—you’d want to duck into a host cell to take some nourishment and replicate under cover, invisible to passing patrols. But this entails work—and risk. The host cell may commit suicide, leaving you vulnerable to passing macrophages, or the host may evolve a defense, as in the case of the resistance to malaria conferred by sickle-cell disease. Gulbins and Lang study pathogen–host cell invasion interactions in hope of developing treatments for infectious disease that mimic host-cell resistance, and thus prevent the development of drug resistance that hampers the effectiveness of antibiotics.