ArticleCell host & microbe2025
Cryptosporidium modifies intestinal microvilli through an exported virulence factor.
Article in Cell host & microbe, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Therapeutic Efficacy of Carvacrol-Loaded Mesoporous Silicate Nanoparticles Against Cryptosporidiosis.Pharmaceutics · 2026Article
- Article
- The genome sequence of the gastric gland parasite,iScience · 2026Article
- Cryptosporidium secreted proteins form a complex layered interface with the host cell.PLoS pathogens · 2026Article
- Infectious Diarrhea in Early Childhood across the Global South: Etiologic Diversity and Pathogenic Mechanisms.ACS infectious diseases · 2026Review
- Insights into the lifecycle of Cryptosporidium and compounds targeting developmental stages.Current opinion in microbiology · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Article
- Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens.PLoS pathogens · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 a 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 localize to the microvilli. We examine the trafficking and function of the most highly expressed family member, Microvilli protein 1 (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.
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Registered trials
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