S. M. Beverley

This study shows that parasite hybridization in cutaneous leishmaniasis increases the spread of endosymbiotic viruses, contributing to disease severity.

This study develops and applies RNAi tools to Leishmania (Viannia) species, showing that RNAi efficacy increases with stem length and enables hypomorphic analysis of essential genes.

This paper uses ultradeep proteomics to analyze Leishmania major mutants, revealing significant proteomic changes in LPG2 and FUT1 mutants and highlighting potential therapeutic targets.

This study uses single-cell analysis to show that Leishmania major amastigotes retain lipophosphoglycan (LPG) expression longer in certain host cells, potentially enhancing infectivity.

This study investigates how sphingolipids in Leishmania major protect ergosterol from sterol-binding toxins, showing that ceramide reduces toxin cytotoxicity and enhances amphotericin B efficacy.

This study shows that Leishmania major lacking inositol phosphorlyceramide synthase (IPCS) remains viable and virulent in mice, suggesting SM salvage compensates for IPC loss.

This study shows IgM antibodies facilitate Leishmania genetic hybridization in vitro and in vivo, leading to full genome hybrids and increased genetic exchange.

The paper provides high-quality genome assemblies and gene annotations for 13 Leishmania and related species to study the origins of parasitism.

This study identifies TbFUT1 as an essential mitochondrial fucosyltransferase in Trypanosoma brucei, critical for both bloodstream and procyclic forms and potentially therapeutically relevant across trypanosomatids.

This paper identifies FUT1 as an essential fucosyltransferase in Leishmania, localized to mitochondria, with enzymatic activity required for viability and mitochondrial function.

This paper investigates how Trypanosome Lytic Factor (TLF) and neutrophils interact to reduce Leishmania major infection, showing TLF requires acidic phagosomes and surface glycoconjugates for parasite lysis.

This study shows that 2’C-methyladenosine triphosphate (2CMATP) inhibits Leishmania RNA virus 1 (LRV1) RNA polymerase, leading to viral eradication in Leishmania guyanensis.