L. D. Sibley

This study develops a human air-liquid interface culture system for Cryptosporidium hominis, revealing it induces type III interferon and reduces Rotavirus infectivity.

This study identifies multiple pathways for glucose phosphate transport and utilization in Cryptosporidium parvum, revealing alternative mechanisms for obtaining phosphorylated hexose.

The paper identifies indole metabolites from the microbiota that inhibit Cryptosporidium parvum growth by disrupting host mitochondrial function and parasite mitosome membrane potential.

This study identifies RNF213 as essential for IFN-gamma-mediated restriction of intracellular pathogens like Toxoplasma gondii and Mycobacterium tuberculosis through ubiquitination, independent of autophagy.

The paper screens interferon-stimulated genes to identify RARRES3 as a factor restricting Toxoplasma gondii infection by inducing premature parasite egress.

This study identifies how the parasite Toxoplasma gondii uses the disordered protein TgIST to block STAT1-mediated gene expression by altering STAT1 dimer conformation and preventing activator recruitment.

This study shows that Toxoplasma bradyzoites have reduced calcium and energy stores, limiting their motility and egress, but they can rapidly restore these stores upon release from cysts.

This study identifies INS1 as a protease critical for macrogamont formation and oocyst production in Cryptosporidium parvum, with loss of INS1 reducing virulence in mice.

This study identifies gut metabolites that influence susceptibility to Cryptosporidium infection in neonatal mice, showing that fatty acids affect parasite growth and invasion.

This study identifies a Toxoplasma gondii effector that inhibits necroptosis by modulating host repressor complexes, thereby preventing cell death and promoting chronic infection.

This study identifies novel mutations in Toxoplasma gondii that confer resistance to artemisinin, including mitochondrial genome amplification and changes in mitochondrial function.

This study shows Toxoplasma gondii infection converts NK cells into ILC1-like cells that persist and circulate independently of infection.

This study evaluates anti-malarial drugs for their ability to inhibit Toxoplasma gondii growth in vitro, finding limited effectiveness for most compounds.