Mechanisms that enable wild mice to survive infection with strains of the Toxoplasma gondii parasite virulent enough to kill laboratory mice offer an explanation for how these parasites have been able to persist in the mouse population.
Cooperation theory and a novel synthetic infection system provides a mechanistic understanding of why a seemingly successful disease management strategy can have devastating consequences for infected hosts.
Analysis of epidemiological data reveals that viral loads in newly HIV-1 infected individuals in Uganda have declined for two decades, and evolutionary modelling shows that attenuation of the virus explains this decline.
A fungal effector secreted by the corn smut pathogen increases the virulence of the pathogen by elevating anthocyanin production and reducing lignification in maize.
The horizontal acquisition of virulence plasmids is potentiated by production practices in plant nurseries and is sufficient to transition Rhodococcus from being beneficial to being pathogenic.
A complex that catalyzes the membrane integration of β barrel proteins and a molecular chaperone promote the complete assembly of a bacterial virulence factor in vitro.
During growth in biofilms and host infection, the opportunistic pathogen Pseudomonas aeruginosa employs respiratory heterocomplexes that support extracellular electron shuttling and pathogenicity.
