Our Lab works on parasites and parasitic diseases of companion and production animals. Our lab is currently looking at dewormer resistance in canine hookworms. We are also looking at the prevalence of GI worms and the efficacy of market-available dewormers against these worms in subtropical dairy cattle. Another study is looking into the prevalence of ticks and tick-borne diseases in wild canids in Australia. Our lab also works on proteomics to better understand heartworm disease and its progression in dogs.
"Our laboratory is interested in the study of human pathogens, particularly trypanosomes and also others that cause so-called Neglected Tropical Diseases.
We develop computational tools and produce (and re-use) large data sets to formulate and guide research hypotheses in the quest for new drugs and diagnostics. Chemo- and Bio-informatics, intensive data integration, data mining, and high-throughput assays and experiments are at the core of our research activities.
In particular, we have a special interest in the study of trypanosomes such as Trypanosoma cruzi (Chagas disease)."
Our laboratory studies the protozoan parasite Cryptosporidium parvum, a leading cause of diarrhea in young children and neonatal calves. We utilize molecular genetics, cellular biology and animal models of infection to discover novel aspects of parasite biology, as well as identifying and validating targets for the development of effective therapies against cryptosporidiosis.
My lab works on understanding the molecular mechanisms of merozoites invasion in Plasmodium falciparum, P. ovale and P. malariae. We study the receptor usage by the different parasites as well as evaluate the diversity that exist in the repertoire of antigens deployed during merozoites invasion. We also have interest in delineating mechanisms of immune reaction either driving diseases or protection. We have been studying the drug susceptibility to parasites within the African transmission zones.
The laboratory that I lead specializes in molecular and cellular biology of Toxoplasma gondii, mainly in the role of histone variants in different biological processes: regulation of gene expression, chromatin modulation and DNA damage repair. Our laboratory was the first to characterize a new variant histone (H2B.Z) from T. gondii, and in parallel to its discovery in Plasmodium. We determined the genomic location of this histone and other variant histones of the parasite, their post-translational modifications, their possible role in gene expression, and established different models of DNA damage. Additionally, the lab continue lines of research on heat shock proteins of T. gondii associated with the biology of the parasite. Finally, We evaluate the application of some proteins in the diagnosis of acute toxoplasmosis in pregnant women and newborns with congenital infections.
Our team focuses on the cell and molecular biology of Toxoplasma gondii. Specifically, we are interested in characterizing the proteins and pathways that regulate the propagation of the parasite and its adaptation to various stressors.
Our team works on the evaluation of adequately processed material of both ecto and endoparasitic helminths, from freshwater fish of the various river basins of India. Specifically our focus mainly on morphology, including ultrastructure, systematics and phylogeny of tapeworms (Cestoda), roundworms (Nematoda) and flukes (Trematoda); ecology and life-cycles of aquatic fish helminths, including trematodes (Digenea), with focus on communities of larval stages in freshwater molluscs.
My research goals are related to the study of the protozoan parasite Entamoeba histolytica that causes human amebiasis, which represents a serious public health problem in countries such as Mexico. I am interested in:
The study on the multi-functionality and diversity of the family of Myb transcription factors in Entamoeba; Nuclear proteome analysis of Entamoeba histolytica and Shelterin complex in Entamoeba histolytica.
Interested in marine parasites: ecology, phylogeny and host-parasite coevolution. Currently working in developing methods for cophylogenetic analysis, functional and phylogenetic diversity of parasite communities, and host-parasite bipartite networks. Also interested in evolutionary morphology of monogeneans.
My group aims to decipher transcriptional and epigenetic mechanisms that govern the development of malaria parasites and their interaction with the human host. We use state-of-the-art genomic (e.g. ChIP-seq, ATAC-seq, single-cell RNA-seq) and quantitative proteomic (e.g. DiQ-BioID) approaches to collect high quality data about the Plasmodium epigenome, transcriptome and proteome. Integrative analysis of these datasets together with complementary sets of biochemical and functional experiments will provide important insights into gene regulatory mechanism of the malaria parasite and clues for the development of antimalarial compounds.
My research program is focused on understanding the mechanisms by which malaria parasites interact with their host cells to create a successful intracellular niche for survival. My lab uses genetic and biochemical approaches to dissect the transport mechanisms and secreted effectors that enable the parasite to co-opt its erythrocyte and hepatocyte host cells.
We study structural mechanisms and cell biology of microbes and their interactions with hosts, using integrative approaches including X-ray crystallography, cryo-electron microscopy, cryo-electron tomography, optical microscopy, biochemistry, microbiology and cell biology techniques. One of our projects focuses on microsporidia, a group of single-celled opportunistic fungal pathogens/parasites that infect a wide range of hosts, and can cause fatal infections in immunocompromised patients. We are interested in the cell biology of microsporidia, how it uses a unique ballistic organelle to invade hosts, and host-pathogen interactions that allow it to thrive in a variety of host cells.
We are interested in developing tools that can be used for malaria elimination settings, as we come from a pre-elimination setting with the obvious need and interest arrises. We investigate the functional genome of P. falciparum gametocytogenesis to identify regulatory points to allow gametocyte differentiation and maturation. We translate our findings to identify antimalarial candidates able to target stage-specific processes in the gametocytes through phenotypic viability screens.
We study two different but related questions. First, we want to know how and why the parsaite senses oxygen. We have discovered that both parasite and host oxygen pathways are important for parasite growth and virulence. In the host, parasite uses an oxygen-regulated transcription factor to promote parasite growth and ongoing studies examine what triggers this transcription factor and which of its target genes are important for Toxoplasma growth. In the parasite, oxygen sensing proteins regulate the protein synthesis and degradation and are working on defining why specific proteins are differentially expressed.
Second, we want to know how Toxoplasma affects the central nervous system and how anti-Toxoplasma immune responses function in the central nervous system. These questions are important because Toxoplasma primarily causes disease in the brain and retina. Our work has revealed that when Toxoplasma actively grows in the brain (a condition known as toxoplasmic encephalitis), it causes a massive reorganization of inhibitory synapses. These changes inhibit GABAergic synaptic transmission and this inhibition is a major factor in the onset of seizures in infected individuals. We are defining how the parasite alters these synapses and how these synapses are specifically targeted.
The flagellated parasite Trypanosoma brucei belongs to the class Kinetoplastida, which also includes the other important human pathogens T. cruzi (causative agent of Chagas disease) and Leishmania sp. (leishmaniasis disease). Despite recent progress in the battle against these diseases, continued research into the basic biology of these pathogens is necessary for the identification of new diagnostic and therapeutic angles.
During the cell cycle of these parasites, organelle positioning and segregation show a high degree of coordination and control. Using molecular and cell biology approaches, we are characterizing the composition, the biogenesis and the function of trypanosome specific cytoskeletal structures such as the flagellar pocket collar.
T. brucei is also an excellent model for studying proteins involved in the biogenesis, structure and function of mammalian cilia and flagella, and mutant proteins involved in male infertility."
Our mission is to learn as much as we can about Toxoplasma biology and pathogenesis using the most powerful tools available to us... and to enjoy the process! Our ultimate hope (and already it's worked out this way with a few projects) is to learn something that others can then develop into a product or procedure that proves useful in alleviating suffering from the serious diseases this and related parasites cause. We work on almost all aspects of Toxoplasma biology ranging from questions about how it can invade virtually any vertebrate cell it encounters (truly!) through to how infection sometimes is asymptomatic while other times it is fatal.
We investigate the development of Trypanosoma and Leishmania in the parasitic life cycles and particularly signaling mechanisms that trigger differentiation. The focus is on cAMP signalling and Protein kinase A (PKA) and led to important insight into the evolution of signaling mechanisms. In addition we study regulation of parasite energy metabolism and metabolic adaptation in the life cycle.
The renewal of the therapeutic arsenal against apicomplexan parasites depends on the understanding of metabolic pathways that sustain parasite survival within the host and its physiological environment. Our lab thus focuses on understanding how parasites, more particularly Toxoplasma and Plasmodium, acquire lipids and nutrient essential for their propagation and survival within their host cells. We have developed solid expertise in membrane biogenesis, lipid synthesis/trafficking/signalling and established our own in-house metabolomics-lipidomics platform to decipher the complex host-parasite metabolic interactions.
Our main research interest aims at elucidating fundamental aspects of Plasmodium biology. Specifically, we are interested in understanding how parasites integrate and transduce cues from their environment to time their development and how they divide to build large populations in their hosts.
Our laboratory focuses on understanding the molecular, cellular, and organismal adaptations that shape the specialized thermal physiology of mammalian-parasitic nematodes. For this work, we use the potentially fatal skin-penetrating human parasite Strongyloides stercoralis and the closely related rodent parasite Strongyloides ratti as model systems. We also use the free-living model nematode C. elegans, which shares many of the same genes and neurons as parasitic nematodes, but exhibits fundamentally different thermosensory behaviors. Research in our lab is driven both by curiosity about the adaptations that generate specialized behavioral repertoires from evolutionary conserved neural circuits, as well as the potential to develop new approaches to treating or preventing helminth infections.
The Bunnik Lab is interested in basic parasite biology centering on the schizont-to-ring transition. We study naturally acquired immune responses against merozoite antigens and use monoclonal antibodies isolated in the lab to gain insight into the function of various merozoite proteins. We also study the regulation of gene expression during this transition stage, with a focus on the epigenetic landscape and the role of ApiAP2 transcription factors in the process of egress and re-invasion.
Our lab is interested in the role of malaria parasite exported proteins in host-parasite interactions. The overall goal with the research in our lab is to better understand the molecular mechanisms through which parasite exported proteins interacts with its host. We do so by primarily using the rodent malaria parasite Plasmodium berghei in vivo infection model. We develop and use high-throughput genetic screens at combine pooled transfections and barcode or gRNA sequencing technology to accelerate our understanding of parasite gene function.
Dr. Cano´s research involves the many aspects implicated in the molecular biology and biochemistry of Leishmania telomeres. The main focuses are i) to identify and functionally characterize the components of the telomeric chromatin and ii) the biogenesis of the telomerase ribonucleoprotein complex, with the aim of discovering in these structures new drug targets or strategies to control and eradicate leishmaniasis. Dr. Cano´s group have already described some proteins that associate in vitro and in vivo with the G-rich single-strand and with the telomeric double strand DNA. Also, they described and functionally characterized some of the components of the telomerase RNP complex such as the TER (RNA component), the TERT (protein component), Hsp90 and PINX1. More recently, the group described how the telomeric LncRNA (TERRA) is expressed during parasite development and continued in vitro passages and are actually studying the roles TERRA plays at parasite telomeres.
In our research group we study the molecular and behavioral parameters that are key to the ability of Anopheles mosquitoes to transmit malaria, with special emphasis on reproductive biology and vector-Plasmodium interactions. Our aim is to provide crucial knowledge to aid the development of new, effective tools for mosquito and malaria control. A key component of our research includes fieldwork studies in Africa on mating biology and natural malaria infections. These studies, in collaboration with IRSS in Burkina Faso, ICIPE in Kenya and other partners, are expanding our understanding of mosquito reproductive biology, mosquito-microbiota interactions, and natural malaria infections.
Dr. Chakrabarti's current research examines global and mechanistic aspects of RNA biology in unicellular parasites. Major focuses are on molecular pathways that regulate functions related to genome integrity and translational control in blood-borne pathogens, Plasmodium falciparum (Malaria) and Trypanosoma brucei.
How is the malaria parasite Plasmodium falciparum able to establish a chronic, asymptomatic infection in a human host? Our team is addressing this question using blood isolates collected in the field and Next Generation Sequencing technology. We are particularly interested in parasite antigenic variation.
Laboratory of Red Cell Diseases investigates blood cell pathologies arising from systemic diseases, oxidative/chemical damage, and microbial infectious agents such as Plasmodium spp., the causative agent of Malaria. Using a combination of proteomics, mechanobiology, and chemical biology, we aim to elucidate novel pathways and candidates for drug and vaccine discovery against infectious agents of tropical relevance. An exciting new direction of the lab aims to understand molecular determinants underpinning host tropism of Plasmodium spp., with overarching implications in parasite adaptations, zoonosis, and progressive drug resistance.
We study Trypanosoma cruzi gene expression, in particular we are interested in TcHMGB, the T. cruzi ortholog of the High Mobility Group B protein and its role in transcription, DNA replication and repair.
We are also interested in TcHMGB function as an immune mediator and its putative implication in Chagas disease pathogenesis.
Our research focuses on genetic and genomic approaches to identify the underlying genetic causes of phenotypic differences between malaria parasite strains. We use the rodent malaria parasites for some of these studies, but we are increasingly pursuing investigations involving the human malaria parasites in in vitro culture. We work in malaria endemic countries on epidemiology related projects, including with P. falciparum and P. vivax in Africa, P. knowlesi and P. cynomolgi in Southeast Asia, and P. simium in Brazil
Our lab (DNA Replication and Repair Laboratory) is interested in studying the DNA metabolism of trypanosomatids etiological agents of Neglected Tropical Diseases (NTDs), named Trypanosoma cruzi (causative agent of Chagas disease), and Leishmania spp. (causative agents of leishmaniases).
We study the molecular mechanisms underlying the different types of DNA damage, focusing on Homologous Recombination repair (HR), Base- Excision Repair (BER), and Nucleotide Excision Repair (NER).
In particular, we have a special interest in the study of Inositol pyrophosphates, which are responsible for pyrophosphorylate proteins that participate in several pathways related to DNA metabolism.
The Debler Lab investigates epigenetic mechanisms of gene regulation in the protozoan parasite Trypanosoma brucei, the causative agent of sleeping sickness. Using an interdisciplinary approach including structural biology, biochemistry, and cell biology, we focus on gene-regulatory mechanisms underlying life-cycle stage control (differentiation) and immune evasion in T. brucei. Investigation of trypanosome biology offers both the potential for important global health impact and an opportunity to explore fascinating eukaryotic biology.
Our work has centered in the characterization of metabolic pathways in protozoan parasites. We currently work with Trypanosoma cruzi, the etiologic agent of Chagas disease, and Trypanosoma brucei, which belongs to the group of parasites that cause sleeping sickness and Nagana. Our ultimate goal is to discover metabolic pathways in these parasites that may be essential for their survival but may not find an equivalent counterpart in their host. Thus, it would be possible to look for specific inhibitors of such metabolic activities as possible means of controlling the parasites without damaging the hosts. We study calcium homeostasis, and polyphosphate metabolism, and their importance for parasite physiology. We are also interested in signaling pathways since there is evidence that these pathways have important roles during the developmental cycle of these parasites. In particular, we became interested in the study of mitochondrial calcium transport.
My research program is focused on understanding how the trypanosomatid parasites undergo morphogenesis, the process they employ to shape their cells and transmit shape during cell division. This is an important question for two reasons: 1. Trypanosomatids have evolved unique approaches for fundamental cellular processes such as morphogenesis; identifying the molecular mechanisms will provide a better understanding of evolutionary niches, such as parasitism, that arise through diversification of cellular pathways in manners that would be extremely difficult to predict; 2. These pathways represent unique and essential aspects of trypanosomatid biology that could be exploited to develop treatments for a range of neglected tropical diseases that cause significant human suffering in developing countries.
We work on the molecular biology of transcription and DNA repair in Plasmodium falciparum. Our focus is on the basic biology of RNA (including mRNA, lncRNAs and mRNA stability), transcription, chromatin structure and nuclear organization. Much of our work is directed toward understanding the process of antigenic variation, including the regulation of var gene expression. We also work on telomere biology and DNA repair.
We are interested in how Plasmodium gametocytes transmit from humans to mosquitoes. Specifically, how does a quiescent mature gametocyte prepare for explosive onward development in the mosquito? We also dream up new ways to prevent this, with the aim of halting malaria transmission and the spread of drug resistance.
In Our lab, we study different aspects of Trichomonas vaginalis pathogenesis.
Cell, molecular and structural biology of P. falciparum membrane proteins. We focus on ion channels and transporters with an emphasis on understanding the protein's structure-function and advancing small molecule inhibitors to antimalarial therapies.
Our research focuses on the cell biology of Leishmania infection. We are interested in the mechanisms underlying biogenesis, development, and function of the Leishmania-containing parasitophorous vacuoles, as well as in the impact of Leishmania infection on host cell mitochondrial biology.
We work on host-parasite interactions with an emphasis on nematode parasites of mammals and insects. As part of this work we study proteins, peptides, and small molecules released by nematodes during infection and evaluating their effects on host biology. We also are interested in lipid signaling during parasite infection.
We are interested in understanding how the sexual stages of the malaria parasites, gametocytes, develop and interact with different tissues and sites of the human host. We study gene expression and immune response of the host against these transmission stages. We use a range of modern molecular, cell biological, transcriptomic, genomic and immunological approaches to understand fundamental parasite biology and immunology and use this knowledge to identify and develop targets for disease intervention.
We are a structural biology lab working on several SET domain containing lysine methyltransferases as well as multiple skeletal protein complexes in human parasites including Trypanosoma brucei, Toxoplasma gondii, and Plasmodium. The approaches we use to address these scientific questions include molecular biology, biochemistry, biophysics, structural biology, etc. We employ the three state-of-the-art structural study methods (X-ray crystallography, NMR spectroscopy and electron microscopy) to determine 3D structures of target biological macromolecules. We also routinely use homology modeling, small angle X-ray scattering (SAXS), static/dynamic light scattering (SLS/DLS), circular dichroism (CD), isothermal titration calorimetry (ITC), and many other techniques in our studies. Our structural studies are often coupled with site-directed mutagenesis, in vitro biochemical experiments, and in vivo assays to validate our mechanistic hypotheses.
Toxoplasma gondii widely infects human population. Approximately, one-third of the human population is infected with Toxoplasma parasites. As an obligate intracellular parasite, Toxoplasma has to invade host cells, replicate, and egress to infect another host cell. My lab focuses on two questions of Toxoplasma infection.
1) How Toxoplasma uses its proteases to disseminate infection?
2) How Toxoplasma acquires and utilizes nutrients from host cells?
Using a combination of molecular biology, biochemistry, and cell biological approaches, my laboratory will study these two questions at molecular and cellular levels. Our work will shed light on the development of novel strategies to specifically block the proteolytic activity and the nutrient acquisition within the parasites to benefit clinical management of infection.
I am a molecular and computational biologist focused on understanding the evolutionary biology of parasitic worms that infect humans and animals. I lead a multidisciplinary research group where we use population-wide to single-cell resolution genomic approaches to understand the genetic mechanisms and phenotypic traits underpinning parasite adaptation and persistence.
Maria’s lab aims to determine how whipworms invade, colonise and persist in the gut. Using a new model she developed based on “mini-guts”, the first to mimic whipworm infections in a lab dish, together with microscopy and sequencing, they are characterising: 1) the molecular and cellular changes that happen in the whipworm and the gut lining and surrounding cells when the parasite enters and colonises the gut and; 2) the interactions that allow the parasite to persist and the gut lining to repair during chronic infections. This knowledge will open new avenues to eradicate whipworm infections and control gut inflammatory diseases.
Our laboratory studies the biology of host-parasite interactions during malaria and babesia blood-stage infections. We are defining essential parasite and red blood cell determinants required for invasion, intracellular growth, pathogenesis and transmission of these debilitating human pathogens.To explore biological questions in both the lab and the field, we develop and use a variety of experimental approaches. We rely on reverse and forward genetics, combined with cell biology, chemical biology, post-genomic and computational approaches. We have long-standing strong collaborations with investigators in disease-endemic countries. The identification of critical molecules and pathways for pathogenic infection can inform vaccine and drug development.
We are broadly interested in answering fundamental questions about the cell biology of Plasmodium parasites.
Our long-term goal is to find new therapeutics to halt parasite replication -- either by finding small molecule inhibitors or new vaccine antigens to block critical parasite processes. We hope to achieve this goal by understanding the functions of novel and essential parasite genes.We are currently focused on the mechanisms of cell division, cell shape, and signaling in the parasite.
Our research interests are Clinical & Diagnostic Human and animal Parasitology, particularly, neglected parasitic diseases, especially that have interface on one health. We are primarily focused on molecular diagnostics and genotypic variance analysis of human parasites that have great impact on human health (Intestinal protozoa (Giardia, Entamoeba, Cryptosporidium, Toxoplasma, Trichomonas…). We also have ongoing interest in novel herbal therapeutics of parasitic diseases. Recently Parasitism and COVID-19 vaccines: new challenge.
My research group studies host-pathogen interactions in malaria, with a focus on understanding host erythrocyte factors important for the biology and pathogenesis of Plasmodium falciparum. We use a variety of approaches spanning molecular parasitology, human stem cell biology, genetics, biochemistry, cell biology and population genetics (e.g. Science 2015, 348: 711-714; eLife 2021, 10e61516; eLife 2021 10:e69808). Stanford University offers a world-class academic environment and a vibrant and large community of postdoctoral fellows (http://postdocs.stanford.edu/).
We study structural mechanisms and cell biology of microbes and their interactions with hosts, using integrative approaches including X-ray crystallography, cryo-electron microscopy, cryo-electron tomography, optical microscopy, biochemistry, microbiology and cell biology techniques. One of our projects focuses on microsporidia, a group of single-celled opportunistic fungal pathogens/parasites that infect a wide range of hosts, and can cause fatal infections in immunocompromised patients. We are interested in the cell biology of microsporidia, how it uses a unique ballistic organelle to invade hosts, and host-pathogen interactions that allow it to thrive in a variety of host cells.
Our research interests are Clinical & Diagnostic Human Parasitology, particularly, neglected parasitic diseases, especially that have interface on one health. We are primarily focused on molecular diagnostics and genotypic variance analysis of human parasites that have great impact on human health (Intestinal protozoa (Giardia, Entamoeba, Cryptosporidium, Blastocystis…), Leishmania, Toxoplasma, Wuchereria bancrofti…). We also have ingoing interest in microbiomes, novel therapeutics of parasitic diseases and vector & vector borne diseases.
Our lab uses a tripartite system consisting of three model organisms: an insect, Drosophila melanogaster; the entomopathogenic (or insect pathogenic) nematode Heterorhabditis bacteriophora; and its symbiotic bacterium Photorhabdus luminescens, in order to investigate the molecular and evolutionary basis of insect immunity, bacterial symbiosis/pathogenicity and nematode parasitism, and to understand the basic principles of the complex interactions between these important biological processes. This system promises to reveal not only how pathogens evolve virulence but also how two pathogens can come together to exploit a common host.
The unifying factor across all our research interests lies in the evolutionary adaptation of the African trypanosome to its host and vector. Our studies have revealed that constant motility is crucial for removing host antibodies from the parasite's cell surface. To enable this process, the primary surface proteins have been intricately designed for enhanced mobility, even operating at the molecular crowding threshold. Our investigations have demonstrated the remarkable speed of endocytosis in trypanosomes, facilitating swift uptake and destruction of immune effector molecules. We utilize sophisticated techniques, including high-end physical, chemical, cell biological, and genetic methodologies. Our toolkit spans from single-molecule tracking and advanced tissue engineering to integrated microfluidics and AI-powered simulation technology.
In our group, we study mechanisms of unconventional protein secretion in two intestinal parasitic protists called Giardia lamblia and Entamoeba histolytica.
We aim to employ a range of methods to determine the composition, phylogenetic history and structural identity of molecular machinery involved in the secretion of parasitic virulence factors. These molecules cause damage to the parasitized host and are often secreted unconventionally using mechanisms that are currently unknown.
Our laboratory is focused on the genomics of parasitic nematodes. Specifically, we are interested in adapting inexpensive whole genome sequencing approaches to better understand the epidemiology and transmission dynamics of these important parasites.
Our research program tackles global problems through local initiatives. Focused on parasitic infections and rooted in the One Health approach, this initiative leverages the power of local communities and global collaboration to advance innovative solutions. The CFP lab focuses on antimicrobial resistance (AMR) in parasitic diseases, particularly Leishmania. Our research explores compensatory adaptations driving drug resistance and targets key functions in neglected tropical diseases (NTDs). We also investigate the role of extracellular vesicles (EVs) in AMR, developing EV-based profiles for early detection of resistance.
Our lab is interested in studying the biology of Plasmodium to identify novel points of attack that can lead to novel antimalarial or vaccine development. As such, we use a wide range of functional and reverse genetic approaches and employ novel molecular tool development to accomplish these goals. We are interested in understanding the host-pathogen interactions present during blood-stage infection of Plasmodium falciparum by characterizing the essential process of host-cell remodeling.
Parasitism relies on the ability of an organism to exploit its host. African Trypanosomes are unicellular parasites responsible for a fatal disease in humans (sleeping sickness), and for a chronic disease in cattle (nagana). We are interested in understanding the cellular and molecular mechanisms employed by these parasites to survive in the mammalian host. We study two main mechanisms: tissue tropism and antigenic variation.
Last year we won the prize for the World's coolest parasitology lab. Check it out:
https://youtu.be/W9bDh5Ww9u0
In our lab we are fascinated by how Plasmodium falciparum employs sophisticated networks of interacting proteins and regulatory non-coding RNAs to control the organization and expression of its genome. To study these processes, we use a multidisciplinary approach combining state-of-the-art genetics, epigenomics, biochemistry and imaging technologies. The ultimate goal of our research is to understand how the parasites can control their cell cycle progression, by translating adaptive signals from their environment into changes of chromatin structure and gene expression.
Hi, I’m Anat, a proud member of the Florentin lab!
We are a group of molecular parasitologists who frame scientific questions in the context of global health. Our lab studies the cell biology and genetics of P. falciparum in order to identify new drug targets and understand the molecular mechanisms of this important pathogen. We see science as a lens through which to see the world, as well as a tool through which to promote progress, social justice and strengthen societal infrastructure.
Our lab brings all these elements into play. It is a place to do science for the sake of its beauty. A platform to develop tools to advance human health. And a nourishing and inclusive environment for people to grow scientifically, professionally and personally. Please check our lab website (below) to read more and connect!
We work on basic cell biology, molecular epidemiology and genomics of apicomplexans, with a focus on Toxoplasma gondii and Neospora caninum. We are particularly interested in understanding the underpinnings of cell division and transmission. We love microscopes and all things related, nanopore flow cells, mutagenesis and biochemistry. We actively collaborate with the clinic and farmers, bringing together basic science and the field. We also deeply love coffee!
We study the different forms of the malaria parasite in the mosquito and how it is transmitted using reverse genetics in rodent-infecting Plasmodium berghei. We also try to develop new methods to generate attenuated parasites for experimental vaccinations. Over the years, we have introduced a number of microscopy and biophysical techniques to parasitology and still marvel at the beauty of this little beasts.
Cells usually proliferate by duplicating their genome and subsequently dividing into two daughter cells. The malaria-causing parasite Plasmodium falciparum proliferates by a remarkably different mode called schizogony. Here, multiple rounds of DNA replication and closed nuclear division occur, forming a multinucleated cell before daughter cells assemble. Although the nuclei reside in a shared cytoplasm, they replicate their DNA and divide independently and asynchronously. This apparent autonomy of the nuclei and the underlying molecular mechanisms are poorly understood. By employing different imaging modalities, paired with molecular genetic, chemical and proteomic tools as well as computational models, we aim to elucidate the limits of nuclear autonomy and discover its molecular determinants.
With a creative, collaborative, biophysical mindset, we aim to understand the ability of parasites to interface with their host-cell to a point at which we can exploit the mechanisms not only for finding cures against the disease the parasites cause but also to make parasite mechanisms a tool that we can use to engineer the host’s cells. By developing approaches that allow a quantitative understanding and manipulation of molecular transport our research transforms parasites from agents of disease to tools for health.
Specifically, we are studying how the malaria parasite takes control over red blood cells. By learning the biophysical principles of transport in between the host and the parasite we can design ways to kill the parasite or exploit it to reengineer red blood cells. The transport we study is broadly encompassing everything from ions, to lipids and proteins. We use variations of quantitative microscopy and electrophysiology to gain insight into the unique strategies the parasite evolved to survive.
Dr. Gazzinelli’s research program has been focused on the regulation of the immune response to helminth parasitic infections and to the pathogenesis of allergic diseases. The Gazzinelli Lab has a specific interest in understanding the plasticity and specificity of circulating peripheral and tissue-resident effector Th2 cells driven by helminth antigens and/or allergens, as well as to understand the role of the effector Th2 subsets in the establishment of tissue Type-2-mediated inflammation using both mouse models and human studies. These studies aim to identify potential targets for the development of selective immunotherapy that could prevent chronic helminth infection or that could diminish allergic inflammation.
Apicomplexan parasites use simplified division patterns in order to multiply efficiently and quickly while producing a large number of parasites. The mechanisms allowing the control and coordination of these modes of division are therefore essential to the survival of these parasites in their hosts. We study the proteins that control and coordinate the division of these parasites, using Toxoplasma gondii as a model Apicomplexa. We are particularly interested in transcription factors of the ApiAP2 family which coordinate specific expression profiles during the cell cycle. In addition, we also study the centrosome, which serves as a platform coordinating the cell cycle. These studies could lead us to better understand the mechanisms of division in this family of parasites in order to develop new molecules aiming at controlling their proliferation.
We use functional genomics approaches to understand how the Leishmania parasite is equipped to complete its life cycle and cause disease in humans and animals.
Focus areas are the structure and function of the flagellum, the role of membrane transporters in intracellular parasites and identification of key virulence factors through forward genetic screens. Our work involves cell culture, microscopy, CRISPR-Cas9 gene editing, screening of CRISPR KO libraries, and a variety of other molecular and biochemical methods.
GEPAMOL is a multidisciplinary research group dedicated to the study of toxoplasmosis (biological, medical and epidemiological aspects) and other pathogenic protozoan diseases (cryptosporidiasis, giardiasis and blastocistosis). Our group work in the development of methods to monitor pathogenic protozoa in food and water.
In ocular toxoplasmosis we study its epidemiology, clinical characteristics and the immune response.
We are also analyzing natural products for its in vitro anti- Toxoplasma activity and we look for vaccine candidates for human toxoplasmosis.
I mentor undergraduate research projects on the biochemistry of the trypanosomatid Crithidia fasciculata and the free-living ciliate Vorticella. We study the contractile vacuole, osmoregulation, and sugar metabolism, as well as student-designed parasitology projects based on their ideas and interests. Together with Swati Agrawal (U. Mary Washington) and Paul Ulrich (GA State) I teach a collaborative, multi-institutional, and cross-disciplinary Course Undergraduate Research Experience. (Note: I currently am not the PI on parasitology grants, but am an assistant professor with active research).
Our team is part of the ESCAPE laboratory, bringing together entomologists, helminthologists, and protistologists to advance parasitology research. We focus on coccidia, including Toxoplasma gondii, Cryptosporidium spp., and Eimeria spp.. Our research involves screening chemical compounds for anti-parasitic activity, identifying target proteins through advanced bioinformatics analyses, and employing transgenic approaches to elucidate host-pathogen interactions and parasite biology. Additionally, we are adapting complex in vitro systems, such as organoid-based air-liquid interface systems, to study parasites with limited in vitro models.
I am a parasitologist holding the associate professor position at the Institute of Maritime and Tropical Medicine of the Medical University of Gdansk in Poland. I specialize in parasitology and rodent-borne diseases. My interests include parasite ecology, host-pathogen interactions and emerging infectious diseases. I lead national and international research projects focusing on biodiversity, intrinsic and extrinsic factors influencing parasite prevalence and abundance in rodents and searching for novel vectors and reservoirs for pathogens. I am a member of the World Health Organisation NTD-STAG Working Group on Monitoring, Evaluation and Research.
Toxoplasma cell division, host cell invasion, comparative biology
Our specific research questions include:
How do parasites physically divide by internal budding?
For signaling purposes, does mitosis complete before the onset of cytokinesis?
What is the function of the basal complex in mature parasites?
How do parasites secrete organelles in a calcium dependent fashion?
What genetic changes underlie lab-adaptation of parasites?
Rapid cell division is critical for the proliferation of malaria-causing parasites in the human blood and during other life cycle stages, but remains poorly understood. Our vision is to generate an extensive cell biological and genetic framework to dissect critical events during nuclear division. The study of this highly dynamic and small scale process requires exquisite temporal and spatial resolution. Hence, we are using a combination advanced imaging techniques such as live cell, super-resolution and correlative light and electron microscopy to study key elements of the division machinery. Ultimately, we hope to uncover which mechanisms regulate the high number of daughter cells that can emerge from a single parasite cell.
Toxoplasma gondii is a common unicellular eukaryotic parasite that causes toxoplasmosis, a foodborne zoonotic disease that can be life-threatening in immunocompromised individuals and the unborn fetus. The team is focused on elucidating the molecular mechanisms by which Toxoplasma evades immune defenses and survives for life in a variety of hosts. We are studying how Toxoplasma employs sophisticated mechanisms to i) profoundly alter the cells it infects to promote parasite persistence, and ii) remodel its own genome to maintain transmission between different hosts. Along the way, we have discovered new antiparasitic agents that effectively prevent acute toxoplasmosis and other apicomplexa-mediated diseases such as malaria and cryptosporidiosis.
Working in the field of infectious diseases principally Leishmania vectors are extremely important and considered a research priority. My work since more than ten years ago was concentrated with molecular biology and population genetics of Phlebotomus papatasi; the Leishmania major vector. I believe that characterizing sand fly populations using good markers like microsatellites and Cyt. B will lead to evaluate the involvement of these populations in Leishmania transmission. Population analysis of P. papatasi may answer important questions about the compatibility of local populations of the parasites with their correspondent vectors and if there is a reciprocal selection between them. Major development has been made during my research carrier in this field; more microsatellite markers have been developed this year and currently genotyping these markers on global collections of P. papatasi is taking place.
We are interested in the uptake, regulation and metabolism of iron by the apciomplexan parasite Toxoplasma gondii. We use molecular and genetic approaches to investigate the role of iron transporters, and their regulation, within the parasite. By understanding how the parasites are manipulating this essential element, we hope to learn more about the metabolism of these obligate parasites.
My lab studies the neural basis of sensory behaviors in skin-penetrating parasitic nematodes. Our work focuses primarily on the human-parasitic nematode Strongyloides stercoralis, the closely related rat-parasitic nematode Strongyloides ratti, and the free-living nematode C. elegans as a comparative model. The overall goal of our research is to understand how parasitic worms use host-associated and environmental sensory cues to locate and invade human hosts.
The focus of the Heaslip Lab is to understand the mechanisms of vesicle trafficking and secretion in Toxoplasma gondii. An acute T. gondii infection is caused primarily by the parasites lytic cycle involving: (1) invasion into the host cell, (2) replication within a specialized vacuole termed the parasitophorous vacuole (PV) and (3) host cell egress and dissemination, which results in the destruction of the infected cell. Invasion and egress depend on secretion of proteins from specialized secretory organelles called the micronemes and rhoptries, while intracellular survival requires secretion of proteins from the dense granules. Protein trafficking to the secretory organelles must be tightly controlled to ensure that the correct complement of proteins is delivered to each secretory organelle. We use a combination of parasite genetics, live cell imaging and single molecule biophysics to address how the actin cytoskeleton and associated myosin motors controls vesicular trafficking and organelle positioning in T. gondii.
Research in our lab focuses on understanding how membrane protein complexes mediate host-pathogen interactions in malaria parasites. We uses single-particle cryoelectron microscopy (cryoEM) to determine near-atomic resolution structures of novel protein complexes that we enrich directly from malaria parasites, and in situ cryoelectron tomography (cryoET) to directly visualize these protein complexes at the host-pathogen interface in parasite-infected erythrocytes at sub-nanometer resolution. To accomplish this, we develop and apply novel approaches that combine cutting-edge techniques in malaria parasite gene-editing, single-particle cryoEM, and in situ cryoET to overcome longstanding barriers to high resolution structural study in malaria parasites.
The Hovel-Miner lab at George Washington University uses genetic tools as their foundation to understand the biology, pathogenesis, and therapeutic approaches to Trypanosomatid parasites. We have developed a state-of-the-art forward genetics tool to connect parasite phenotypes to their genes and pathways in the form of an ORFeome-based Gain-of-Function library for Trypanosoma brucei. The Gain-of-Function library permits diverse genetic screens to identify genes whose expression promotes specific phenotypes. Specifically, we have focused on identifying genes that promote drug resistance and are actively conducting screens and evaluating the outcome of screens that identify drug mechanisms of action and resistance mechanisms. Other areas of specific interest include mitochondrial redox metabolism, which has been implicated in our drug resistance screens, and mechanisms of DNA break repair. T. brucei employs antigenic variation to evade host immunity, a process underpinned by DNA break formation and repair by recombination. While aspects of DNA metabolism are conserved in trypanosomes, compared with other eukaryotes, missing enzymes and regulatory factors need to be identified. Projects in the lab include novel drug and compound screening using the Gain-of-Function library, evaluating the effects of identified drug resistance genes on mitochondrial functions, and molecular mechanisms of DNA break repair and antigenic variation in T. brucei.
The Huet lab uses Toxoplasma gondii to investigates the highly divergent metabolic adaptations of apicomplexan parasites. We use genetic, biochemical and cellular approaches combined with metabolomics and proteomics to study the unique aspects of the apicomplexan endosymbiotic organelles. Our research aims to understand the highly divergent biology of those subcellular structures to reveal phylum-specific adaptations and possible vulnerabilities as therapeutic targets.
Tonay INCEBOZ, a senior lecturer in Medical Parasitology, has graduated from Ege University of Medical Faculty (Turkey) in 1988, and completed his Med. PhD in Medical Parasitology at the same university in 1998. He became associate Professor in 2008, and Professor in 2014. He is currently working as a professor in the department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.
I have a special interest with your work and would like to serve as a research assistant in your laboratory. I’m very much interested of working on Trichomonas vaginalis (diagnosis, PCR and invitro cultivation) and Echinococcus granulosus and Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation and diagnosis, Western blot, PCR).
My research focuses on capacity building and pathogen genomics, with a specific focus on the surveillance of parasite populations, antimalarial drug resistance and efficacy of antimalarials. I am leading several collaborative projects which are investigating the genomics of malaria parasites, human genome variations and rare diseases in Tanzania. I am a member of different associations and networks, including the Genomic Epidemiology of Malaria Network (MalariaGEN), US President's Malaria Initiative-Supported Antimalarial Resistance Monitoring in Africa Network (PARMA) and ASTMH.
The next generation of interventions against malaria depends on a deep understanding of the biology of Plasmodium and the complex relationships established with the human host and the mosquito vector. We explore this in the lab to discover novel ways to disrupt parasite growth and to characterize new antigens for diagnosis or vaccination. We especially focus on the function of carbohydrate-active enzymes and on the glycobiology of P. falciparum. Due to the common location of glycans (i.e. carbohydrate chains) in the cell surface and their important roles, the study of glycoconjugates constitutes a fertile ground for the discovery of drug targets and molecules with vaccine and diagnostic potential.
The protozoan parasite Toxoplasma gondii is estimated to infect over 2 billion people worldwide, including approximately 20% of Americans. This highly prevalent parasite is adept at establishing a long-term chronic infection that can reactivate to cause serious acute disease in immunocompromised or pregnant people. Although there are some limited treatments available to treat this acute stage of the infection, these therapies often cause toxic side effects, or allergic reactions and can be unsuitable for use in vulnerable patients. Furthermore, the chronic stage of the parasite is currently incurable.
The goal of the Jeffers lab is to understand how the parasite activates or “switches on” gene expression to drive parasite growth and transition in its life cycle and cause disease. This complex process is influenced by a variety of factors, but we are currently interested in epigenetic mechanisms of control, specifically the contribution of bromodomain proteins. These proteins “read” gene activation marks on the chromatin to recruit other complexes that regulate transcription. Determining the role of the bromodomains in regulating Toxoplasma gene expression is not only a fascinating biological question but could also contribute to the development of more effective anti-parasitic drugs. We are now extending our interests in parasite gene expression to investigate precisely how the bromodomain proteins directly regulate the transcriptional initiation machinery and the factors that are necessary to activate a gene. We use an array of genomic, proteomic, molecular and cellular biology approaches to answer these questions.
We are interested in understanding the role that ion channels play in sensing of external and internal conditions in protozoan parasites. We focus our work in the biophysics and physiology of mechanosensitive, potassium and calcium channels, and how they affect the fitness and infectivity of Trypanosoma cruzi, Trypanosoma brucei and Toxoplasma gondii. Our long-term goal is to exploit unique characteristics of these channels for the development of selective therapeutic approaches against parasitic diseases.
Our research interests focus on the molecular epidemiology, population genetics, transmission, and environmental biology of livestock-related protozoa as well as other emerging zoonotic pathogens. Additionally, our work includes the study of vector-borne tropical diseases and Wolbachia-based biological control of mosquito vectors. Currently, we are conducting molecular investigations on Cryptosporidium, Toxoplasma, Giardia, Enterocytozoon, and Blastocystis in children and farm animals in Bangladesh.
Malaria is a major health issue, with drug-resistant parasites complicating control efforts. My lab investigates the epigenetic and transcriptional mechanisms underlying drug resistance and antigenic variation in malaria parasites. We generated a comprehensive map of histone modifications in P. falciparum and identified intergenic enhancer-like elements. Recently, we developed a single-cell RNA-seq atlas, suggesting that cellular homeostasis plays a role in stress survival and drug resistance. We also report high rates of transcriptomic single-nucleotide variations (SNVs). Our studies highlight PfGCN5 and PfHDAC1 as key regulators in artemisinin resistance. Also, we are interested in studying field isolates and whole-genome sequencing to understand the genomic basis of artemisinin resistance.
The Kissinger Research Group focuses on genome evolution in parasitic protists. Projects include organellar genome evolution, gene transfer, population genomics and evolution of gene regulation in the Apicomplexa. Our interests also include data integration, data sharing, data mining and data visualization challenges in support of research.
The malaria research group of the Department of Medical Microbiology of the Radboudumc (Nijmegen, Netherlands) consists of four closely-interacting core teams covering the entire breadth of malaria research: field & transmission (Bousema), immunology & CHMI (Mordmüller/McCall), transmission-blocking vaccines (Jore), molecular & cellular biology (Kooij). We also have close interactions with the malaria epigenetics group (Bártfai; Radboud University) and the innovative spin-off TropIQ.
In my group, we use a murine in vivo model and in vitro cultured human malaria parasites for functional profiling throughout the complex life cycle. We develop and employ tools for larger-scale experimental genetics combined with advanced flow cytometric and microscopical techniques. Furthermore, we are increasingly integrating experimental and computational approaches to predict and validate the organellar proteomes and essential roles of the identified proteins in mammalian and mosquito hosts. One of are latest innovations is the development of Plasmodium complexome profiling, which we are using to study stage-specific functioning of mitochondrial protein complexes. In my lab and in collaboration with local and international colleagues in academia and industry, we will thus shed light on fundamental parasite biology during host-transitions, fueling our joined fight against malaria by strengthening the search for prophylactic and transmission-blocking intervention strategies.
The Kowalinski group is keenly interested in gene expression regulation through RNA processing complexes. We study the unusual mRNA processing pathways in Trypanosoma brucei using X-ray crystallography and cryo-EM. We combine these structural biology methods with scattering techniques like small-angle X-ray scattering (SAXS), biophysical methods, biochemical assays, computational structure prediction, and cell biology.
The major focus of my work is to decipher the molecular mechanisms underlining sexual stage differentiation and gamete fertility in the malaria parasite Plasmodium falciparum. These stages and underlying processes are critical for parasite transmission to the mosquito vector. Another line of research in my lab is to understand the mechanism of drug resistance in P. falciparum.
Research in the Kyle lab focuses on the discovery, development, and mechanism(s) of resistance to anti-parasitic drugs. At present we focus on malaria, the most important parasitic disease of man, and the spectrum of diseases caused by pathogenic free-living amoebae, perhaps the most neglected of all tropical parasitic diseases. The overarching objectives of our research are to develop new tools to prevent disease, to train a new generation of parasitologists, to foster multidisciplinary research on tropical diseases, and to implement our findings to reduce the burden of parasitic diseases in endemic countries.
Research in my laboratory focuses on the study of signal transduction pathways in trypanosomes, flagellated protozoan parasites that belong to the Kinetoplastida order. Integrating cellular, biochemical and genetic approaches the Lander lab investigates the mechanisms by which Trypanosoma cruzi—the etiologic agent of Chagas disease—senses microenvironmental changes and triggers specific cellular responses that lead to differentiation among the main stages of the parasite’s life cycle.
Plasmodium falciparum gametocytes, the sexual stages responsible for parasite transmission from humans to mosquitoes, are key targets for malaria elimination. Immature gametocytes sequester about ten days in the bone marrow and then mature gametocytes are released into the bloodstream where they can persist for several weeks. The Lavazec lab aims to dissect the mechanisms developed by the parasite to sequester in the bone marrow and to persist in the bloodstream. We use experimental approaches combining biophysical and microscopy techniques with cellular biology to decipher the interactions between parasites and bone marrow cells as well as the changes in red blood cell mechanical properties during parasite maturation. The lab has identified parasite proteins and signaling pathways that participate to these processes and has established that these mechanisms may be new targets to block malaria parasite transmission.
My laboratory uses methods in molecular and structural biology (X-ray crystallography, Cryo-electron microscopy, and Nuclear Magnetic Resonance) to characterize the protein synthesis machinery of parasites, such as the ones causing Leishmaniasis, Malaria and Babebiosis, that significantly burden public health. Our long-term goal is to harness this information to develop safe and effective antiparasitic drugs.
Gene regulation, epigenomics, Systems Biology of apicomplexan parasites.
My lab is interested in telomere functions in genome stability and gene expression regulation. We study telomere functions in antigenic variation in Trypanosoma brucei that causes human African trypanosomiasis. T. brucei regularly switches its major surface antigen, VSG, to evade the host immune response, while VSGs are expressed from subtelomeric loci in a monoallelic manner. We have shown that telomere proteins play important roles in antigenic variation. Specifically, RAP1 is essential for VSG monoallelic expression, while TRF, RAP1, TIF2, and PolIE all suppress VSG switching by maintaining telomere integrity. We are also investigating how telomere proteins facilitate telomere replication and help coordinate the telomeric G and C strand syntheses. In addition, we study how telomerase – with a protein subunit, TERT, and an RNA subunit, TR – helps maintain telomere length. Specifically, we are interested in how TR secondary structure and TERT-TR interaction affect telomerase activity.
Our work in the Lindner Lab couples molecular parasitology and structural biology to understand how the malaria parasite (Plasmodium spp.) prepares itself for unpredictable moments where it can transmit between host and mosquito. We focus on the translational repression of mRNAs that are needed in a just-in-time fashion for specific moments before/after transmission. In particular, we are fascinated by the RNA-binding proteins that govern these regulatory processes and the cis elements on mRNAs that make them specific.
The questions being addressed in my lab predominantly center on the red blood cell stage of parasite development, which is the stage in which all of the clinical manifestations of the malaria disease occur. My research focuses on two major areas: the role of transcriptional regulation in orchestrating parasite development, and an in-depth characterization of the malaria parasite’s unique metabolic network. On the transcription side, my lab is dedicated to the characterization of the first family of DNA binding proteins to be identified in the P. falciparum genome, the Apicomplexan AP2 (ApiAP2) proteins. ApiAP2 proteins are considered the major transcriptional regulators of malaria parasite development at all stages of the lifecycle. Our metabolomics work has begun to identify unique biochemical pathway architectures in the parasite. We are now also exploiting our metabolomics approaches to investigate the mode of action of anti-malarial drugs through signature metabolite profiling.
Lo lab studies host-pathogen interactions and evolutionary genomics of malaria parasites Plasmodium in the context of epidemiology and transmission in African countries. My team combines field-based and lab-based molecular biology and ‘omics’ approaches to explore the mechanisms of pathogen invasion and how genome evolution leads to changes in disease dynamics and control measures.
We are interested in:
Finding new treatments and drug-targets for the treatment of acute and chronic toxoplasmosis.
Toxoplasma gondii ultrastructure;
Mechanisms of resistance to drugs of Brazilian isolates of Toxoplasma gondii;
Understanding the pathogenesis of atypical Brazilian isolates of T. gondii in rodents models.
We are currently working on the host parasite interactions at the membrane interface, investigating Plasmodium and Toxoplasma parasite biology and invasion strategies. And investigation of antimalarial activity of medicinal plant extracts from Northeast India region.
Greg Matlashewski is a professor in the Department of Microbiology and Immunology at McGill University. He is a fellow of the Royal Society of Canada and a Fellow of the Canadian Academy of Health Sciences. He is the former leader of the visceral leishmaniasis elimination program at the WHO special program for research and training in tropical diseases (TDR). His research program is centered on using molecular biology and implementation science to find real solutions to support the elimination of leishmaniasis. His current research focuses on generating an attenuated vaccine strain for leishmaniasis through a multidisciplinary approach. He is also performing research to define the genetic basis for different pathologies cause by Leishmania infection.
We study the cell biology of the most virulent human malaria parasite, Plasmodium falciparum. By combining advanced experimental genetics with quantitative microscopy and chemical biology, we gain insights into the fundamental adaptations that safeguard the survival of these fascinating single cell organisms during blood stage development. Our current research work focuses on the digestive vacuole, a highly specialized parasite organelle whose functions are critical for blood stage survival and targets of many antimalarial drugs.
Apicomplexan parasites possess unique organelles, cytoskeletal structures, signalling cascades, replicate by internal budding within a specialised compartment and actively invade and exit the host cell, to name a few aspects of the unique biology that characterise this phylum.
We use reverse and forward genetic tools, combined with cutting edge imaging approaches to investigate and compare the fascinating cell biology of apicomplexan parasites with other model organisms.
Currently we focus our research on the mechanisms involved in host cell invasion and egress and the biogenesis and recycling of the unique secretory organelles.
While our most favourite pet is Toxoplasma gondii, we also study Plasmodium falciparum, Eimeria tenella and Besnoitia besnoiti.
My lab uses 3D spatial metabolomics (chemical cartography) to understand host-parasite-microbiome communication and guide drug development, with a focus on Chagas disease.
The laboratory's research focuses on the study of Plasmodium falciparum resistance to antimalarial drugs. A multidisciplinary approach integrating molecular biology, genomics and clinical studies is used. The goal is to elucidate the underlying mechanisms of resistance and to develop improved diagnostic and therapeutic strategies. We are investigating unconventional parasite resistance mechanisms, such as dormancy in P. falciparum ring stages. In addition, we study the epidemiology of Plasmodium vivax in sub-Saharan Africa, with a particular focus on host-pathogen interactions, especially invasion pathways in Duffy-negative individuals. Our goal is to establish an in vitro culture platform. Through global collaborations and transnational projects, we are improving molecular surveillance systems, enabling early detection of resistant parasites, and strengthening research capacity in endemic regions to advance malaria control and combat drug resistance.
My group studies the human malaria parasite Plasmodium falciparum. Research interests are centred around DNA biology, particularly the molecular mechanisms underlying DNA replication and cell cycle control in Plasmodium, which replicates by an unusual method called schizogony. I am also interested in mechanisms for silencing and promoting the recombination of a family of key virulence genes called var genes - particularly the role that G-quadruplex DNA/RNA structures may play in var gene control, and in the control of other genes as well. We have discovered that G-quadruplexes and their helicases have quite broad roles in genome stability/evolution in the malaria parasite, as well as in gene expression. Finally, I have a long-standing interest in epigenetics, for example in a group of NAD+-dependent deacetylase enzymes called sirtuins which regulate subtelomeric chromatin and virulence gene expression. My postdoctoral work linked the Plasmodium falciparum sirtuins to particular patterns of var gene expression and to severe malaria in human patients.
In my laboratory we work with two experimental models, Trypanosoma evansi and Trypanosoma vivax. Using proteomic analysis, we intend to describe the proteins found and study the possibility of using any of them as biomarkers and/or diagnostic targets. We also worked with the vectors of these parasites.
I am interested in defining the molecular genotypes and signatures associated with drug resistance in the malaria Plasmodium falciparum parasite across diverse genetic backgrounds. My research employs systems-based multi-omics and genetic approaches to identify genetic determinants of antimalarial drug resistance, understand the molecular mechanisms underpinning resistance, and characterize the impact of these resistance-associated mutations on the parasite’s physiology, including fitness and transmission.
Research in the Muralidharan lab is aimed at understanding the biology of Plasmodium, the deadly human parasite that causes malaria. Our research focuses on organelle biology in this deeply branched eukaryote. We are particularly interested in the organization and function of the secretory pathway in two parasite specific biological processes: 1. The export of parasite effectors to the host red blood cell. 2. Egress of the parasite daughter cells from the infected red blood cell.
The main objective of this project is to deepen the understanding of helminthiasis and perform One Health based parasitological screening comprising humans, livestock, wild animals, and environment in Bangladesh. This study will also explore the barriers and gaps of current parasitic disease control strategies and looks for an approach that can be implemented with minimum resources.
We are studying in vitro and in vivo antiplasmodial activity of plant extracts in order to produce a phytodrug
The Ochsenreiter Lab is working in the field of molecular biology, using the single-celled parasite model system Trypanosoma brucei to uncover the principles that govern mitochondrial biogenesis, including organelle fusion and fission, mitochondrial genome replication, segregation, as well as mitochondrial gene expression. To address our questions, we use a range of different techniques, including:
immunofluorescence microscopy
superresolution microscopy - expansion microscopy
electron microscopy and cryo electron tomography
proximity labeling techniques
proteomics and next generation sequencing
molecular biology
Martin Olivier, Ph.D., has been an Immuno-Parasitologist and Full Professor at the Departments of Medicine, Microbiology, and Immunology at McGill University and the Research Institute of the MUHC for the last 22 years. He is the Director of the Laboratory for the Study of Host-parasite Interaction. His work uses cell biology, molecular biology, immunology, and Omics to study the pathogenesis of malaria, leishmaniasis, and viruses (Ebola, HIV, Phlebovirus, LRV1). His findings in host-pathogen interaction, pathogen evasion mechanisms, innate immune response, exosome biology and sandfly nanobiome, have been reported in over 200 papers. His research has translated into the development of nanovaccine technology, anti-inflammatory molecules and immunomodulators. His actual main interest is the study of extracellular vesicles/exosomes of Leishmania and their role in the modulation of Leishmania fitness and their impact on the host innate inflammatory response and macrophage signaling and functions.
Dr. Sabine Ottilie is the program manager of the MalDA Consortium, an innovative drug discovery platform that aims to deliver antimalarial lead compounds against novel targets.
The aim of MalDA is to improve and accelerate the early antimalarial drug discovery process by identifying new, essential, druggable targets. In addition, it seeks to produce early lead inhibitors that may be advanced into drug candidates suitable for preclinical development and subsequent clinical testing in humans. By sharing resources, including expertise, knowledge, materials, and reagents, the consortium strives to eliminate the structural barriers often encountered in the drug discovery process.
The Pawlowic lab studies Cryptosporidium, a parasite that causes diarreheal disease in young children and immunocompromised adults. We use genetics and biochemistry to understand how the parasite is transmitted. We are also developing new tools for Mode of Action studies and drug discovery for the treatment of cryptosporidiosis.
We study signalling mechanisms that underpin malaria parasite transmission. We are particularly interested in how post-translation modifications regulate gametocyte development and onward activity in the mosquito.
My lab studies metabolic pathways in Plasmodium and Trypanosoma brucei to understand gene essentiality and pathway regulation. We use the knowledge gained by our biochemical and structural biology approaches to foster drug discovery programs for both organisms. In particular we have targeted dihydroorotate dehydrogenase for the treatment of malaria, and have focused on the polyamine, as well as purine and pyrimidine pathways in T. brucei.
The research we conduct is directed toward a main objective: achieving elimination of this disease from Cambodia. While amazing progress has been done for Plasmodium falciparum, the situation is strikingly different for Plasmodium vivax that requires dedicated intervention, and therefore research, to be eliminated. Our work combines mechanistic questions on the basic biology of host-parasite interactions with very operational research projects in order to develop and implement approaches for the control and elimination of malaria
In the lab we aim to understand how Plasmodium falciparum survives the dry season when no mosquitoes are available. We study the host and parasite factors that contribute to silent carriage of parasites in ~20% of children during the 6-month dry season in Mali, and how transmission resumes in the ensuing wet season when mosquitoes return. With samples from cohort studies implemented in close collaboration with a Malian team of clinical and lab researchers, and multiple visits to Bamako we search the molecular mechanisms that help parasites persist.
We do molecular cellular biology to understand the immunopathogenesis of Taenia solium in neurocysticercosis.
I am interested in infectious and zoonotic diseases in wildlife and domestic animals. My current research focuses the epidemiology of Trichomonas spp. in wild birds and the environment, molecular detection of Sarcocystis spp. in avian brain tissue, the prevalence of other infectious diseases in wildlife, and pathogens detected from environmental samples.
We study host-pathogen interactions, cell-cell interactions, cell death and repair, focusing on the pathogenic amoeba Entamoeba histolytica. E. histolytica causes amoebiasis, a potentially lethal diarrheal disease. The species was named “histolytica” (histo-: tissue; lytic-: dissolving) for its ability to injure host tissue. We showed that E. histolytica amoebae kill human cells by trogocytosis (trogo-: nibble), in which they ingest human cell “bites.” Trogocytosis contributes to tissue damage and it provides a new paradigm for amoebiasis pathogenesis. Trogocytosis also enables amoebae to acquire and display human cell membrane proteins, facilitating immune evasion. In addition to its contribution to disease, as an unusual cell killing insult, trogocytosis further provides a vehicle to uncover new human cell death and survival signaling. There is also an emerging appreciation that many eukaryotes perform trogocytosis, suggesting that it might be fundamental to eukaryotic biology.
I have dedicated the last 18 years of my career developing molecular tools and genomic analyses for tracking the dispersal and evolution of Trypanosoma cruzi, Blastocystis and Leishmania. The efforts of my lab are evidenced in more than 190 research articles published in international journals and more than 20 supervised Bachelor, Master and PhD students. As both a laboratory director with expertise in microbiology and a tropical infectious disease specialist, my background and extensive experience have led me to build a robust interdisciplinary background in endemic and emerging parasitic diseases. Currently, I am an associate professor at the Universidad del Rosario in Bogota, Colombia, and the Icahn School of Medicine at Mount Sinai in New York City, USA.
Strikingly, in all humans there are three subtypes of high-density lipoprotein (HDL, the good cholesterol), which are defined by their ability to kill African Trypanosomes that cause Nagana in animals. Two components, haptoglobin-related protein, and APOLIPOPROTEIN L1, which are not found in bulk HDL and are unique to Trypanosome lytic factors (TLFs), are instrumental in lytic activity. After ingestion of TLFs, APOL1 forms pH gated ion channels in the plasma membrane of the parasites, resulting in ion flux, osmotic swelling, and lysis. Subspecies of trypanosomes that are resistant to lysis by TLF can infect humans causing sleeping sickness. Genetic variants of APOL1, G1 and G2, evolved in Africa to combat human infective trypanosomes. However, chronic kidney disease in African Americans is associated with the HIGH expression of these two variants. The molecular cause of kidney cell death is due to the formation of APOL1 pH gated ion channels and can be stopped with channel blockers.
We study how the competition between Toxoplasma and its varied hosts has driven the evolution of signaling molecules on both sides of the host pathogen interface. To do this, we combine methods in molecular genetics, cell biology, biophysics and structural biology to deeply interrogate problems from the organismal level down to atomic levels of detail.
My research program is focused on the study of the biology of parasitism and host-parasite interactions using molecular biology and genomic approaches with the ultimate goals to better understand parasitic lifestyle and infection and identify new targets for diagnosis and for prophylactic and therapeutic interventions. We have studied the responses of human cells to the infection, showing that T. cruzi reprograms human cells, and we propose that host targeted therapies can be also used in Chagas diseases. We study the genome organization of T. cruzi, and showed that this genome is composed of a core and disruptive compartment, the latter being the source of diversity in the interaction with hosts since it contains the main multigene families, composed of surface proteins coding genes.. Similar approaches are in course in other protozoan parasites (Leishmania spp., Neospora caninum).
I have longstanding research interests in parasite cell biology & molecular genetics, working primarily on drug resistance mechanisms, organellar evolution, host-pathogen interactions and differentiation in Toxoplasma and Plasmodium. In recent years my group has worked to provide online bioinformatics resources to the community, facilitating the management, integration and mining of large-scale datasets. I (co-)direct the Eukaryotic Pathogen, Host & Vector Bioinformatics Resource Center (VEuPathDB.org) and the Clinical Epidemiology Resource ClinEpiDB.org.
The Rice Research Group has a broad interest in orphan/rare infectious diseases caused by pathogenic free-living amoebae (pFLA; Acanthamoeba species, Balamuthia mandrillaris, and Naegleria fowleri). All of these pathogens can cause diverse central nervous system (CNS) diseases, Granulomatous Acanthamoeba encephalitis (GAE) , Balamuthia amoebic encephalitis (BAE), and primary amoebic meningoencephalitis (PAM), respectively. These CNS diseases all have >92% fatality rates, which is alarming for any patients diagnosed or afflicted by such diseases.
Our lab has experience in drug discovery up to pre-clinical in vivo efficacy models, which we routinely run to identify the next partner therapeutics. We are always accepting new collaborations and partnerships within our discovery interest!
The Rijo-Ferreira lab at UCBerkeley studies circadian rhythms in parasitic diseases. We are currently focusing on malaria parasites, trying to understand the molecular basis for parasites synchronization within the blood stage for their 24h rhythms. We are interested in the host, the parasite and mosquito clocks.
My lab major is the study of malaria parasites. We have an excellent track record in parasite cell biology, molecular biology and biochemistry, providing contributions to the advancement of drug discovery and development, vaccines and host-pathogen interactions. We are also interested more broadly in infectious diseases and their pathophysiological traits in general (with a clear bias towards parasites), including viruses and bacteria. As time goes on, it becomes more and more fundamentally important to focus some of our efforts on the impact of climate change on infectious diseases and severe outbreaks. We do so by taking an inclusive one-health approach encompassing plants, insects and animal infections.
We are interested in host-parasite interactions between the obligate intracellular eukaryotic parasite Toxoplasma gondii and its mammalian hosts. The focus of my laboratory over the last years has been to identify genes of Toxoplasma that determine virulence, host genes and pathways that determine resistance/susceptibility, and to characterize their specific interactions. To achieve this we use a combination of genomics, biochemistry, genetics, microscopy, immunology and computational tools.
For 40+ years I have studied the cell biology and biochemistry of human pathogens that cause liver fibrosis (Schistosoma mansoni), dysentery (Entamoeba histolytica), diarrhea (Giardia lamblia and Cryptosporidium parvum), birth defects (Toxoplasma gondii) and blindness (Acanthamoeba castellani).
In experiments currently funded by an R01 from NIGMS, we are studying the effects on acute and chronic mouse infections (model for human infection), as well as cat infection (host that makes infectious oocysts), of knockouts of the Toxoplasma gene that encodes an O-fucosyltransferase (TgSPY), which modifies nucleocytosolic proteins involved in protein and mRNA transport between the nucleus and cytosol. We are also studying the effects on a mouse model of human infection of knockout of the Cryptosporidium gene encoding a nucleocytosolic O-fucosyltransferase (CpSPY).
In other experiments for which we anticipate funding, we are studying the structure and assembly of cyst walls of Acanthamoeba. These walls contain cellulose and xylan (like plants) and chitin (like fungi), as well as a remarkable set of lectins that have unique chitin-binding domains.
Techniques in the lab include super-resolution microscopy for localization of proteins and glycopolymers, mass spectrometry for identification of O-fucosylated and cyst wall proteins, AlphaFold for structure/function experiments, and CRISPR/Cas9 for gene knockouts.
Our goal is to understand how the human malaria parasite Plasmodium falciparum transcriptionally commits within the host cell, the erythrocyte. The research team uses molecular, genetic and cellular approaches to identify and characterize parasite transcription factors, in order to identify possible new drug targets.
In the Schulz lab, we use the African trypanosome as a model system to understand how organisms reprogram themselves in response to changes in their environment. African trypanosomes are the causative agent of sleeping sickness in humans and nagana in cattle. Sleeping sickness is fatal if untreated, and the economic burden due to losses in livestock is estimated to be over $2 billion per year in regions of Sub-Saharan Africa where the disease is endemic. African trypanosomes are protozoan parasites that are transmitted to the mammalian host through the bite of the tsetse fly. We aim to understand how the parasites adapt to different environments in the fly and mammalian bloodstream, with an eye toward manipulating this adaption to help fight disease.
Melanie is committed to the goal of eradicating malaria. Her aim is to undertake translationally relevant research that directly informs development of the next generation of malaria vaccines. Melanie leads the University of Washington non-human primate malaria vaccine research program with colleague Dr. Sean Murphy. Her research also includes malaria vaccine antigen discovery and studies in rodent malaria models.
My lab uses a systems biology approach to study trypanosomes and to pursue the long-term research goals of (1) deciphering how various environmental stimuli and intracellular cues regulate different functional aspects of the kinetoplastid mitochondrion, (2) investigating how the metabolic status of the mitochondrion dictates parasite differentiation, and (3) targeting regulatory mechanisms conserved between kinetoplastid parasite species to identify potential pan-kinetoplastid drug targets.
My laboratory works on the molecular and cell biology of Toxoplasma gondii. The lab currently has 3 NIH-funded projects. The first deals with the development and implementation of imaging based approaches to gain insights into the biology of tissue cysts and the bradyzoites within them (posters at this meeting presented by 1: Anthony Sinai and 2: Cortni Troublefield. A second project aims at dissecting the role of amylopectin granules in the chronic infection. The third project aims to dissect the functional contribution of ubiquitination focused how deubiqutinases control cell cycle architecture (poster at this meeting presented by Seth McConnell). My lab is open to recruiting a postdoc with interests in these areas.
Je travaille sur le paludisme transfrontalier entre l'Algérie, le Niger et le Mali. J'étudie le plasmodium et le vecteur l'anophèle lui même. Actuellement je travaille avec mon équipe sur l'élaboration d'une nouvelle technologie pour lutter contre le vecteur mais aussi l'élaboration d'une nouvelle molécule à partir des plantes médicinales traditionnelles pour le traitement du paludisme.
Google translation:
I work on cross-border malaria between Algeria, Niger and Mali. I study the Plasmodium and the vector anopheles itself. Currently I am working with my team on the development of a new technology to fight against the vector but also the development of a new molecule from traditional medicinal plants for the treatment of malaria.
We study epitranscriptomic pathways, including tRNA modification reprogramming, and epigenetic stress response pathways in drug resistant malaria parasites. We also seek to identify epigenetic and epitranscriptomic drivers of entry into and exit from drug- and starvation-induced parasite quiescence.
The major focus of our work is to decipher the molecular mechanisms underlining gliding motility, host cell invasion and egress in the obligate intracellular parasites Toxoplasma gondii. This journey led us so far to the molecular dissection of myosin motors, actin dynamics, adhesins, proteases and more recently lipid signaling mediators and secretory organelle biogenesis and exocytosis. We aim to better understand host-parasite interactions in general, from host-cell recognition to development in the intracellular niche. In the recent years we have become increasingly engaged in malaria research and initiated some studies on the metabolic pathways hosted by two endosymbiotic organelles, the mitochondrion and the relic of a plastid called the apicoplast. Some of these questions are also addressed to the more challenging encysted stage of T. gondii which is central to parasite persistence and transmission.
The Sinnis Laboratory is part of the Johns Hopkins Malaria Research Institute, committed to the pursuit of basic science research that translates into solutions targeting one of the most important infectious diseases in the world. Our research focuses on the infective stage of the malaria parasite, sporozoites, which are inoculated into the skin by infected mosquitoes. Using biochemical, cell biological, and genetic approaches as well as intravital imaging and proteomics, we aim to understand the molecular interactions between sporozoites and their mosquito and mammalian hosts that enable the parasite to initiate infection. Recently we have started investigating the quantitative dynamics of sporozoite transmission, an understudied yet important area of inquiry if we are to improve our epidemiologic models and define the minimum efficacy required of transmission blocking interventions.
The Steinel Lab’s focus is in understanding the interplay and co-evolution of hosts and pathogens. Using threespine stickleback (Gasterosteus aculeatus) and Schistocephalus solidus as a model organism, the lab studies teleost adaptive immunity, the manipulation of adaptive immunity by parasites, and the co-evolution of host and parasite factors. This work involves both laboratory-based experimentation as well as the study of wild populations.
My team focuses on three themes: the study of the fundamental biological processes of trypanosomatids, genomics, and translational research (molecular diagnosis of Toxoplasmosis and Leishmaniasis). We also spend lots of time to develop tools to study our favorite nasty Parasites: FISH, DNA combing, CRISPR-Cas9, inducible CRISPR-Cas9 and SNS-seq
We study regulatory mechanisms governing life cycle stage transitions in the apicomplexan parasite Toxoplasma gondii. In this context, we study cellular signaling, epigenetics, transcription factors, translational control, and epitranscriptomics. We also examine experimental therapeutics targeting latent toxoplasmosis and the behavior changes associated with chronic infection.
My lab is dedicated to the experimental and computational application of cryo-ET for structural determination of biological macromolecules or biological machinery in single-celled parasites that cause important human diseases. I am particularly interested in understanding the molecules transportation, organelle biogenesis and their regulations in the invasion process of the malaria parasites and the migration of Trypanosoma brucei that causes African sleeping sickness in humans and Nagano in cattle. Our research is to visualize the organization of cellular structures and their coordination in 3D spatial organization through a multi-scale imaging platform ranging from microns to sub-nanometers, to elucidate the molecular and structure functions that drive cell migration or invasion.
My team’s research focuses on uncovering the complexities of parasite-host interactions using advanced bioinformatics and multi-omics techniques, such as genomics, proteomics, and metabolomics. This interdisciplinary work combines computational approaches to create tools for analyzing and visualizing biological data, with the aim of identifying the molecular mechanisms driving parasitic infections. For the past two decades, my primary research has centered on Trichomonas vaginalis, the protozoan parasite responsible for trichomoniasis in humans. Currently, I am investigating how Trichomonasvirus affects the biology of T. vaginalis, as well as exploring the roles of novel microproteins in the parasite’s response to environmental stress.
We study iron-stress response pathways in African trypanosomes; deeply diverged eukaryotic parasites of humans and livestock. We seek to understand (i) how trypanosomes sense, respond, and adapt to changes in host iron availability; and (ii) how trypanosome-specific proteins with non-canonical RNA recognition motifs interact with mRNA to control gene expression in response to nutritional cues.
Parasites are subversive; they bend their environment to their own ends. Plasmodium falciparum and Toxoplasma gondii are two of a large group of single-celled parasites (the Apicomplexa) that invade host cells and hijack the normal biology of those cells to support their own development. Unrestricted growth leads to disease, which is often, but not always, allowed by a weakened or not fully developed immune system.
These two parasites live in very different biological niches, but immune evasion, host cell remodelling, and adaptions to enable transmission between hosts are key to both of their parasitic lifestyles. Our main aim is to determine how the parasites remodel their hosts to for survival, immune evasion, and dissemination. The key tools we use for this are quantitative mass spectrometry, which allows us to interrogate protein interactions and modifications that underpin these processes, and CRISPR-Cas9 based knockout screening, to assess the functional contribution of hundreds of different proteins at the same time. Together with other biochemical, cell biological, and genetic tools, these technologies allow us to uncover exciting and novel biology to build the basis for future therapeutic strategies.
Tsaousis lab current research is focused on the investigations of the adaptations of microbial eukaryotic organisms, and their course in parasitic evolution and diversity. To accomplish this, our laboratory is combining detailed bioinformatics analyses of newly generated genomic/transcriptomic/metabolomic results with field, cell biological and biochemical methods to investigate the parasitic and free-living microbial eukaryotes living in diverse and extreme environments.
My laboratory uses a combination of genetics, cell biology and proteomics approaches to understand biological systems at the molecular level. Our research is primarily focused on the African trypanosomes (Trypanosoma brucei and Trypanosoma congolese) and related species such as Leishmania. We are studying how the parasites are able to sense and respond to their host environment, and aim to translate the results of this basic research into early-stage drug discovery.
My lab focuses on understanding unique aspects of molecular and cell biology of malaria parasites. Over more than 30 years, we have worked on mitochondrial functions in malaria parasites and have collaborated to discover new antimalarials as well as to understand their mechanism of action. We are also working on antimalarials that disrupt Na+ and lipid homeostasis in malaria parasites. These studies are revealing unique pathways and processes of malaria parasites, and pointing to mechanisms of action and resistance to novel antimalarial drugs in development.
How microbes interact with their hosts plays an important role in human and animal health. Especially the microbes in the gut are of crucial importance. We are interested in how these microbes affect human and animal health. Adaptation of microbial eukaryotes to low oxygen, as found in the gut for example, and in particular their mitochondrial adaptations to low oxygen are our major interest. Currently, Blastocystis is our main parasite of interest but more generally, any intestinal parasite is interesting!
Understanding host-parasite-vector interactions during malaria parasite transmission.
Our lab studies the epigenetic and transcriptional control mechanisms that regulate clonally variant phenotypes in the malaria parasite Plasmodium falciparum, particularly antigenic variation and sexual commitment. We are also interested in elucidating various aspects of gametocyte biology and transmission, and in developing and applying tools for transmission-blocking drug discovery.
The Wang lab’s long-term research goals are understanding the innate immune machinery determining Toxoplasma resistance between different hosts and demonstrating the molecular basis of Toxoplasma effector-mediated host immune modulation. Activating such anti-Toxoplasma machinery or inhibiting the immunomodulatory parasite effectors could sensitize the parasite to immune surveillance and lead to a better treatment against Toxoplasma infection in immunocompromised patients. To achieve the goals, Wang lab applies a multifaceted approach, including functional genomics, proteomics, bioinformatics, and other biochemical analysis.
We are working to understand the mechanisms underlying T. gondii motility and host cell invasion. We study motility at multiple levels, from the biophysical properties of the myosin motor that drives forward motion, to how the parasite navigates complex 3D environments, to the consequences of disrupting motility in mouse models of infection. Our studies of invasion are currently focused on the signaling pathways triggered when the parasite engages a host cell and the mechanism by which the engaged parasite injects rhoptry proteins into the host cell to manipulate host cell behavior.
The Wetzel lab studies trypanosomatid parasites including Leishmania and T. brucei.
Our research interests fall under 2 broad categories:
1. Host-pathogen interactions – Questions we ask include the following:
How does Leishmania enter cells? How does it survive in phagocytic cells? How
does it spread from host cell to host cell? How do differences in these processes affect disease in animal models and humans? Our ultimate goal is to use what we learn about parasite pathogenesis to suggest new host-directed therapies for leishmaniasis.
2. Drug discovery – We have identified several promising antileishmanial lead compounds from phenotypic and target-based drug screens. One compound that we identified preferentially facilitates tubulin polymerization within parasites. Ongoing studies are directed at defining its mechanism of action. We also have an active medicinal chemistry campaign to identify derivatives of this compound that are effective in mouse models of leishmaniasis and trypanosomiasis.
We are always looking for excellent new lab members! If you would like to apply, please contact me at dawn.wetzel@utsouthwestern.edu
Our group is interested in translational research and finding new treatments for malaria and the discovery of druggable targets. I am the director of the Malaria Drug Accelerator, an international consortium focused on finding new treatments for malaria (https://MalariaDA.org). We are also interest in the genetics and genomics of malaria parasites.
My group is focused on determining the mechanism of action (MoA) and/or molecular targets of compounds that are phenotypically-active against the parasites that cause neglected tropical diseases. We use a matrix of established and new methodologies in the fields of high-throughput genetics, cell biology/biochemistry and chemical proteomics to facilitate our MoA studies. The principal goal of the group is to feed much-needed chemically-validated drug targets into drug discovery programmes to facilitate target-based drug discovery. In uncovering the MoA of these compounds, we have the potential to identify exploitable drug targets and the ability to generate chemical and biological tools that can be used to study fundamental parasite biology.
Glycosylation is one of the most common biochemical events occurring in all living organisms. Glycomics studies have revealed that parasitic nematodes synthesize and modify their proteins with a repertoire of glycan structures (carbohydrates), which are very different from the ones in mammals. On one hand, these “foreign” nematode glycans are antigenic to the host, contributing to the elevation of anti-parasite antibodies upon infection; on the other hand, nematode-derived glycoproteins interact with immune cells, leading to remarkable immunoregulatory effects on the hosts. My research focus is primarily on 1) identifying novel glyco-epitopes on the glycoproteins of parasitic nematodes, 2) characterising novel glyco-enzymes involved in nematode glycan biosynthesis and, 3) glycoengineering and recombinant expression of parasite glycoproteins with biopharmaceutical potential.
I am a demonstrator of medical Parasitology at faculty of medicine, Sohag University. I am working on a research for Entamoeba histolytica parasite to compare the validity of Immunochromatography Vs the microscopy in Entamoeba diagnosis
The central ambition of our laboratory is to combine molecular, genetics, and computational approaches to make discoveries that improve our understanding of helminth parasite biology and host-parasite interactions, as well as our ability to treat parasitic infections. This includes identifying new targets for drug discovery, elucidating of mechanisms of drug resistance, and developing new tools for parasite manipulation and phenotypic screening. We directly study human and animal helminths, including mosquito-borne filarial nematodes, soil-transmitted nematodes, and snail-transmitted blood flukes. To complement these efforts, we leverage the powerful model organism Caenorhabditis elegans.
My lab utilizes Trypanosoma brucei, a powerful model organism to study cell differentiation and adaptability to different environmental stimuli. This parasite naturally progresses through distinct life cycle forms as it adapts to the various nutritional availabilities and temperature differences encountered in the bloodstream of its mammalian host and insect vector. Importantly, it possesses just a single mitochondrion that undergoes striking changes in both its energy metabolism and mitochondrial ultrastructure throughout the parasite life cycle. One of the main topics in the lab is to elucidate how the metabolic rewiring of T. brucei generates mitochondrial signals that are propagated throughout the cell to drive parasite differentiation. Another focus of the lab centers on the relationship between mitochondrial ultrastructure and the bioenergetics of the FOF1-ATP synthase dimers.