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.

Hysteretic switching between virulence states has been observed in a human pathogen.

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.

Receptor recognition of antimicrobial peptides is important for Salmonellae to survive inside macrophages and cause disease.

Gene knockout of liver fluke granulin by CRISPR/Cas9 attenuates the virulence of infection with a carcinogenic liver fluke.

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 acquisition of a virulence plasmid is sufficient to turn a beneficial strain of Rhodococcus bacteria into a pathogen.

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.

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.