Host DNA

Interferons (IFNs) are released by mammalian cells upon attack by microbial pathogens, alerting neighboring cells to prepare a defense that includes the activation of so-called IFN-stimulated genes. Although this response nearly always limits viral replication, its role during bacterial infection has not been clear. In some cases, the IFN response accelerates bacteria clearance, but in other cases, it results in a more severe disease (1, 2). The latter is true for Listeria monocytogenes, the bacterium that causes a range of human illnesses, from gastroenteritis to fatal meningitis. On page 1319 of this issue, Lebreton et al. (3) identify a new virulence factor, LntA, secreted by L. monocytogenes, that controls the expression of IFN-stimulated genes. The mechanism allows the bacterium to govern both the induction and repression of the host cell immune response, perhaps to optimize conditions for specific stages of infection or colonization of specific tissues.