Elena Rodrigues
elena-l-r.bsky.social
Elena Rodrigues
@elena-l-r.bsky.social
Postdoc at the Francis Crick Institute in the Sateriale lab. Working on virulence factors of Cryptosporidium!
Reposted by Elena Rodrigues
A fun little review of convergent mechanisms in pathogenesis 🦠 We really enjoyed putting this together and I think it comes through on the page @elena-l-r.bsky.social @ghostpathogen.bsky.social & Mitch Pallett dx.plos.org/10.1371/jour...
Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens
The epithelial layer that lines the digestive system serves as the primary barrier to infection by intestinal pathogens. While this layer has evolved complex molecular mechanisms to identify and respo...
dx.plos.org
August 1, 2025 at 9:56 AM
Reposted by Elena Rodrigues
Crick researchers have uncovered how the intestinal Cryptosporidium parasite uses a protein to alter its host’s gut environment, enabling the parasite to survive and replicate.

www.crick.ac.uk/news/2025-04...
Researchers uncover how intestinal parasite Cryptosporidium alters host cells
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...
www.crick.ac.uk
April 29, 2025 at 2:37 PM
Reposted by Elena Rodrigues
Cryptosporidium modifies intestinal microvilli through an
exported virulence factor!! Phenomenal work from the newly DR’ed Elena Rodrigues
www.biorxiv.org/content/10.1...
Cryptosporidium modifies intestinal microvilli through an exported virulence factor
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.
www.biorxiv.org
February 26, 2025 at 12:53 PM