Costs of Illness in the 1993 Waterborne Cryptosporidium Outbreak, Milwaukee, Wisconsin

Researchers at the Francis Crick Institute have shown that the Cryptosporidium parasite exports a protein into infected intestinal cells, altering the gut environment and enabling the parasite to surv...

An arrayed microscopy-based CRISPR screen revealed host genes affecting multiple infection phenotypes of the intracellular parasite Cryptosporidium. Hits in the host cholesterol biosynthesis pathway a...

Cryptosporidium is a common intestinal infection of vertebrates and a significant threat to public health. Within the epithelial layer of the intestine, the parasite invades and replicates. Infected cells are readily detected under the microscope by the presence of elongated microvilli, particularly around the vacuole where the parasite resides. Here, we identify a family of Cryptosporidium virulence factors that are exported into the host cell during infection and localise to the microvilli. We examine the trafficking and function of the most highly expressed family member, MVP1, which appears to control the elongation of microvilli through engagement of host EBP50 and CDC42. Remarkably, this mechanism closely mirrors that of an enteropathogenic Escherichia coli virulence factor, MAP, which is also known to drive host microvilli elongation during infection. This highlights a unique instance where eukaryotic and prokaryotic virulence factors have convergently evolved to modulate host actin structures through a similar mechanism. ### Competing Interest Statement The authors have declared no competing interest.