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7. Sol-gel processing of a covalent organic framework for the generation of hierarchically porous monolithic adsorbents

Author

Carrington, Mark E., Rampal, Nakul, Madden, David G., O’Nolan, Daniel, Casati, Nicola Pietro Maria, Divitini, Giorgio, Martín-Illán, Jesús Á., Tricarico, Michele, Cepitis, Ritums, Çamur, Ceren, Curtin, Teresa, Silvestre-Albero, Joaquin, Tan, Jin-Chong, Zamora, Felix, Taraskin, Sergei, Chapman, Karena W., and Fairen-Jimenez, David

Published
2022
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10. How are Trypanosoma brucei receptors protected from host antibody‐mediated attack?

Author

Banerjee, Sourav, Minshall, Nicola, Webb, Helena, and Carrington, Mark

Subjects
TRYPANOSOMA brucei, MORPHOLOGY, CELL receptors, CYTOLOGY, AFRICAN trypanosomiasis, TRANSFERRIN, HAPTOGLOBINS
Abstract

Trypanosoma brucei is the causal agent of African Trypanosomiasis in humans and other animals. It maintains a long‐term infection through an antigenic variation based population survival strategy. To proliferate in a mammal, T. brucei acquires iron and haem through the receptor mediated uptake of host transferrin and haptoglobin‐hemoglobin respectively. The receptors are exposed to host antibodies but this does not lead to clearance of the infection. Here we discuss how the trypanosome avoids this fate in the context of recent findings on the structure and cell biology of the receptors. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Molecular mechanism of complement inhibition by the trypanosome receptor ISG65.

Author

Cook, Alexander D., Carrington, Mark, and Higgins, Matthew K.

Subjects
*COMPLEMENT inhibition, *COMPLEMENT receptors, *CELL receptors, *COMPLEMENT (Immunology), *COMPLEMENT activation, *BINDING sites, *GRANULOCYTES
Abstract

African trypanosomes replicate within infected mammals where they are exposed to the complement system. This system centres around complement C3, which is present in a soluble form in serum but becomes covalently deposited onto the surfaces of pathogens after proteolytic cleavage to C3b. Membrane-associated C3b triggers different complement-mediated effectors which promote pathogen clearance. To counter complement-mediated clearance, African trypanosomes have a cell surface receptor, ISG65, which binds to C3b and which decreases the rate of trypanosome clearance in an infection model. However, the mechanism by which ISG65 reduces C3b function has not been determined. We reveal through cryogenic electron microscopy that ISG65 has two distinct binding sites for C3b, only one of which is available in C3 and C3d. We show that ISG65 does not block the formation of C3b or the function of the C3 convertase which catalyses the surface deposition of C3b. However, we show that ISG65 forms a specific conjugate with C3b, perhaps acting as a decoy. ISG65 also occludes the binding sites for complement receptors 2 and 3, which may disrupt recruitment of immune cells, including B cells, phagocytes, and granulocytes. This suggests that ISG65 protects trypanosomes by combining multiple approaches to dampen the complement cascade. [ABSTRACT FROM AUTHOR]

Published
2024
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16. The Genome of the African Trypanosome Trypanosoma brucei

Author

Berriman, Matthew, Ghedin, Elodie, Hertz-Fowler, Christiane, Blandin, Gaëlle, Renauld, Hubert, Bartholomeu, Daniella C., Lennard, Nicola J., Caler, Elisabet, Hamlin, Nancy E., Haas, Brian, Böhme, Ulrike, Hannick, Linda, Aslett, Martin A., Shallom, Joshua, Marcello, Lucio, Hou, Lihua, Wickstead, Bill, Arrowsmith, Claire, Atkin, Rebecca J., Barron, Andrew J., Bringaud, Frederic, Brooks, Karen, Carrington, Mark, Cherevach, Inna, Chillingworth, Tracey-Jane, Churcher, Carol, Clark, Louise N., Corton, Craig H., Cronin, Ann, Davies, Rob M., Doggett, Jonathon, Djikeng, Appolinaire, Feldblyum, Tamara, Field, Mark C., Fraser, Audrey, Goodhead, Ian, Hance, Zahra, Harper, David, Harris, Barbara R., Hauser, Heidi, Hostetler, Jessica, Ivens, Al, Jagels, Kay, Johnson, David, Johnson, Justin, Jones, Kristine, Kerhornou, Arnaud X., Koo, Hean, Larke, Natasha, Landfear, Scott, Larkin, Christopher, Leech, Vanessa, Line, Alexandra, Lord, Angela, MacLeod, Annette, Mooney, Paul J., Moule, Sharon, Morgan, Gareth W., Mungall, Karen, Norbertczak, Halina, Ormond, Doug, Pai, Grace, Peacock, Chris S., Peterson, Jeremy, Quail, Michael A., Rabbinowitsch, Ester, Rajandream, Marie-Adele, Reitter, Chris, Salzberg, Steven L., Sanders, Mandy, Schobel, Seth, Sharp, Sarah, Simmonds, Mark, Simpson, Anjana J., Tallon, Luke, Tait, Andrew, Tivey, Adrian R., Van Aken, Susan, Walker, Danielle, Wanless, David, Wang, Shiliang, White, Brian, White, Owen, Whitehead, Sally, Woodward, John, Wortman, Jennifer, Adams, Mark D., Embley, T. Martin, Gull, Keith, Ullu, Elisabetta, Barry, J. David, Fairlamb, Alan H., Opperdoes, Fred, Barrell, Barclay G., Donelson, John E., Hall, Neil, Fraser, Claire M., Melville, Sara E., and El-Sayed, Najib M.

Published
2005

17. The Genome Sequence of Trypanosoma cruzi, Etiologic Agent of Chagas Disease

Author

El-Sayed, Najib M., Myler, Peter J., Bartholomeu, Daniella C., Nilsson, Daniel, Aggarwal, Gautam, Tran, Anh-Nhi, Ghedin, Elodie, Worthey, Elizabeth A., Delcher, Arthur L., Blandin, Gaëlle, Westenberger, Scott J., Caler, Elisabet, Cerqueira, Gustavo C., Anupama, Atashi, Arner, Erik, Åslund, Lena, Attipoe, Philip, Bontempi, Esteban, Bringaud, Frédéric, Burton, Peter, Cadag, Eithon, Campbell, David A., Carrington, Mark, Crabtree, Jonathan, Darban, Hamid, da Silveira, Jose Franco, de Jong, Pieter, Edwards, Kimberly, Englund, Paul T., Fazelina, Gholam, Feldblyum, Tamara, Ferella, Marcela, Frasch, Alberto Carlos, Gull, Keith, Horn, David, Hou, Lihua, Huang, Yiting, Kindlund, Ellen, Klingbeil, Michele, Kluge, Sindy, Koo, Hean, Lacerda, Daniela, Levin, Mariano J., Lorenzi, Hernan, Louie, Tin, Machado, Carlos Renato, McCulloch, Richard, McKenna, Alan, Mizuno, Yumi, Mottram, Jeremy C., Nelson, Siri, Ochaya, Stephen, Osoegawa, Kazutoyo, Pai, Grace, Parsons, Marilyn, Pentony, Martin, Pettersson, Ulf, Pop, Mihai, Ramirez, Jose Luis, Rinta, Joel, Robertson, Laura, Salzberg, Steven L., Sanchez, Daniel O., Seyler, Amber, Sharma, Reuben, Shetty, Jyoti, Simpson, Anjana J., Sisk, Ellen, Tammi, Martti T., Tarleton, Rick, Teixeira, Santuza, Van Aken, Susan, Vogt, Christy, Ward, Pauline N., Wickstead, Bill, Wortman, Jennifer, White, Owen, Fraser, Claire M., Stuart, Kenneth D., and Andersson, Björn

Published
2005

19. A unique mRNA decapping complex in trypanosomes.

Author

Kramer, Susanne, Karolak, Natalia Katarzyna, Odenwald, Johanna, Gabiatti, Bernardo, Castañeda Londoño, Paula Andrea, Zavřelová, Anna, Freire, Eden Ribeiro, Almeida, Kayo Schemiko, Braune, Silke, Moreira, Claudia, Eder, Amelie, Goos, Carina, Field, Mark, Carrington, Mark, Holetz, Fabiola, Górna, Maria Wiktoria, and Zoltner, Martin

Published
2023
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25. Chromatin clues to the trypanosome parasite's uniform coat

Author

Kelly, Steve and Carrington, Mark

Subjects
Chromatin -- Research, Antigenic determinants -- Research, Trypanosoma -- Research -- Physiological aspects, Genomics, Antigens, Trypanosomiasis, Genes, Infection, Genomes, Proteins, Criminal investigation, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The parasite Trypanosoma brucei causes sleeping sickness. It evades human defences by changing the version of a protein that coats its surface. Analysis of its genome and nuclear structure clarifies this variation process. Histone proteins affect the process of antigenic variation in trypanosomes., Author(s): Steve Kelly, Mark Carrington Author Affiliations: Chromatin clues to the trypanosome parasite's uniform coat Most infections don't usually cause prolonged illness in humans because the body's immune system recognizes [...]

Published
2018
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26. Transcriptome, proteome and draft genome of Euglena gracilis

Author

Ebenezer, ThankGod E., Zoltner, Martin, Burrell, Alana, Nenarokova, Anna, Novák Vanclová, Anna M. G., Prasad, Binod, Soukal, Petr, Santana-Molina, Carlos, O’Neill, Ellis, Nankissoor, Nerissa N., Vadakedath, Nithya, Daiker, Viktor, Obado, Samson, Silva-Pereira, Sara, Jackson, Andrew P., Devos, Damien P., Lukeš, Julius, Lebert, Michael, Vaughan, Sue, Hampl, Vladimίr, Carrington, Mark, Ginger, Michael L., Dacks, Joel B., Kelly, Steven, and Field, Mark C.

Published
2019
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27. Evolution of the primate trypanolytic factor APOL1

Author

Thomson, Russell, Genovese, Giulio, Canon, Chelsea, Kovacsics, Daniella, Higgins, Matthew K., Carrington, Mark, Winkler, Cheryl A., Kopp, Jeffrey, Rotimi, Charles, Adeyemo, Adebowale, Doumatey, Ayo, Ayodo, George, Alper, Seth L., Pollak, Martin R., Friedman, David J., and Raper, Jayne

Published
2014

42. A longitudinal two-year survey of the prevalence of trypanosomes in domestic cattle in Ghana by massively parallel sequencing of barcoded amplicons.

Author

Ofori, Jennifer Afua, Bakari, Soale Majeed, Bah, Saikou, Kolugu, Michael Kojo, Aning, George Kwame, Awandare, Gordon Akanzuwine, Carrington, Mark, and Gwira, Theresa Manful

Subjects
CATTLE productivity, AFRICAN trypanosomiasis, CATTLE breeds, CATTLE, TSETSE-flies
Abstract

Background: Animal African Trypanosomiasis (AAT) is one of the most economically important diseases affecting livestock productivity in sub-Saharan Africa. The disease is caused by a broad range of Trypanosoma spp., infecting both wild and domesticated animals through cyclical and mechanical transmission. This study aimed to characterize trypanosomes present in cattle at regular intervals over two years in an AAT endemic and a non-endemic region of Ghana. Methodology/Principal findings: Groups of cattle at Accra and Adidome were selected based on their geographical location, tsetse fly density, prevalence of trypanosomiasis and the breed of cattle available. Blood for DNA extraction was collected at approximately four to five-week intervals over a two-year period. Trypanosome DNA were detected by a sensitive nested PCR targeting the tubulin gene array and massively parallel sequencing of barcoded amplicons. Analysis of the data was a semi-quantitative estimation of infection levels using read counts obtained from the sequencing as a proxy for infection levels. Majority of the cattle were infected with multiple species most of the time [190/259 (73%) at Adidome and 191/324 (59%) at Accra], with T. vivax being the most abundant. The level of infection and in particular T. vivax, was higher in Adidome, the location with a high density of tsetse flies. The infection level varied over the time course, the timings of this variation were not consistent and in Adidome it appeared to be independent of prophylactic treatment for trypanosome infection. Effect of gender or breed on infection levels was insignificant. Conclusions/Significance: Most cattle were infected with low levels of several trypanosome species at both study sites, with T. vivax being the most abundant. The measurements of infection over time provided insight to the importance of the approach in identifying cattle that could suppress trypanosome infection over an extended time and may serve as reservoir. Author summary: Cattle are of economic importance in sub-Saharan Africa as they fulfil multiple roles, ranging from draught power, to providing manure, milk, and meat. However, Animal African Trypanosomiasis (AAT) diseases in cattle affect productivity and food security in most African countries. In Ghana, bovine trypanosomiasis has been detected in few cross-sectional studies by molecular methods. To get a better understanding of the disease, a longitudinal study showing natural trypanosome infection over the life of cattle will be applicable. To explore this issue, the study determined the nature of trypanosome infection in cattle in farm settings in Ghana over two years, a period similar to that used in beef production, by massively parallel amplicon sequencing. The study provided a description of the prevalence over two years and showed that the cattle were infected with multiply species most of the time and the level of infection varied but was low most of the time. The longitudinal study allowed the identification of one individual able to supress infection far more effectively than other members of the herd and this is crucial in implementing control measures in the infected area. [ABSTRACT FROM AUTHOR]

Published
2022
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43. An Alternative Strategy for Trypanosome Survival in the Mammalian Bloodstream Revealed through Genome and Transcriptome Analysis of the Ubiquitous Bovine Parasite Trypanosoma (Megatrypanum) theileri

Author

Kelly, Steven, Ivens, Alasdair, Mott, G. Adam, O’Neill, Ellis, Emms, David, Macleod, Olivia, Voorheis, Paul, Tyler, Kevin, Clark, Matthew, Matthews, Jacqueline, Matthews, Keith, and Carrington, Mark

Subjects
Sucrose, Trypanosoma, Gene Expression Profiling, Cell Cycle, Trypanosomiasis, Bovine, Protozoan Proteins, cell surface components, Trypanosoma theileri, Host-Parasite Interactions, Blood, Animals, Cattle, RNA Interference, Gene Silencing, RNA, Messenger, genome, transcriptome, Genome, Protozoan, Phylogeny, Research Article
Abstract

There are hundreds of Trypanosoma species that live in the blood and tissue spaces of their vertebrate hosts. The vast majority of these do not have the ornate system of antigenic variation that has evolved in the small number of African trypanosome species, but can still maintain long term infections in the face of the vertebrate adaptive immune system. Trypanosoma theileri is a typical example, it has a restricted host range of cattle and other Bovinae and is only occasionally reported to cause patent disease although no systematic survey of the effect of infection on agricultural productivity has been performed. Here, a detailed genome sequence and a transcriptome analysis of gene expression in bloodstream form T. theileri have been performed. Analysis of the genome sequence and expression showed that T. theileri has a typical kinetoplastid genome structure and allowed a prediction that it is capable of meiotic exchange, gene silencing via RNA interference and, potentially, density-dependent growth control. In particular, the transcriptome analysis has allowed a comparison of two distinct trypanosome cell surfaces, T. brucei and T. theileri, that have each evolved to enable the maintenance of a longterm extracellular infection in cattle. The T. theileri cell surface can be modelled to contain a mixture of proteins encoded by four novel large and divergent gene families and by members of a major surface protease gene family. This surface composition is distinct from the uniform variant surface glycoprotein coat on African trypanosomes providing an insight into a second mechanism used by trypanosome species that proliferate in an extracellular milieu in vertebrate hosts to avoid the adaptive immune response.

Published
2017

44. The genome sequence of Trypanosoma cruzi, etiologic agent of Chagas disease

Author

Sayed, Najib M. El-, Myler, Peter J., Bartholomeu, Daniela C., Nilsson, Daniel, Aggarwal, Gautam, Tran, Anh-Nhi, Ghedin, Elodie, Worthey, Elizabeth A., Delcher, Arthur L., Blandin, Gaelle, Westenberger, Scott J., Caler, Elisabet, Cerqueira, Gustavo C., Branche, Carole, Haas, Brian, Anupama, Atashi, Arner, Erik, Aslund, Lena, Attipoe, Philip, Bontempi, Esteban, Bringaud, Frederic, Burton, Peter, Cadag, Eithon, Campbell, David A., Carrington, Mark, Crabtree, Jonathan, Darban, Hamid, da Silveira, Jose Franco, de Jong, Pieter, Edwards, Kimberly, Englund, Paul T., Fazelina, Gholam, Feldblyum, Tamara, Ferella, Marcela, Frasch, Alberto Carlos, Gull, Keith, Horn, David, Hou, Lihua, Huang, Yiting, Kindlund, Ellen, Klingbeil, Michele, Kluge, Sindy, Koo, Hean, Lacerda, Daniela, Levin, Mariano J., Lorenzi, Hernan, Louie, Tin, Machado, Carlos Renato, McCulloch, Richard, McKenna, Alan, Mizuno, Yumi, Mottram, Jeremy C., Nelson, Siri, Ochaya, Stephen, Osoegawa, Kazutoyo, Pai, Grace, Parsons, Marilyn, Pentony, Martin, Pettersson, Ulf, Pop, Mihai, Ramirez, Jose Luis, Rinta, Joel, Robertson, Laura, Salzberg, Steven L., Sanchez, Daniel O., Seyler, Amber, Sharma, Reuben, Shetty, Jyoti, Simpson, Anjana J., Sisk, Ellen, Tammi, Martti T., Tarleton, Rick, Teixeira, Santuza, Van Aken, Susan, Vogt, Christy, Ward, Pauline N., Wickstead, Bill, Wortman, Jennifer, White, Owen, Fraser, Claire M., Stuart, Kenneth D., and Andersson, Bjorn

Subjects
Trypanosoma cruzi -- Genetic aspects, Science and technology
Abstract

Whole-genome sequencing of the protozoan pathogen Trypanosoma cruzi revealed that the diploid genome contains a predicted 22,570 proteins encoded by genes, of which 12,570 represent allelic pairs. Over 50% of the genome consists of repeated sequences, such as retrotransposons and genes for large families of surface molecules, which include trans-sialidases, mucins, gp63s, and a large novel family (>1300 copies) of mucin-associated surface protein (MASP) genes. Analyses of the T. cruzi, T. brucei, and Leishmania major (Tritryp) genomes imply differences from other eukaryotes in DNA repair and initiation of replication and reflect their unusual mitochondrial DNA. Although the Tritryp lack several classes of signaling molecules, their kinomes contain a large and diverse set of protein kinases and phosphatases; their size and diversity imply previously unknown interactions and regulatory processes, which may be targets for intervention., Trypanosoma cruzi causes Chagas disease in humans. Acute infection can be lethal, but the disease usually evolves into a chronic stage, accompanied in 25 to 30% of cases by severe [...]

Published
2005

45. GeneDB—an annotation database for pathogens

Author

Logan-Klumpler, Flora J., De Silva, Nishadi, Boehme, Ulrike, Rogers, Matthew B., Velarde, Giles, McQuillan, Jacqueline A., Carver, Tim, Aslett, Martin, Olsen, Christian, Subramanian, Sandhya, Phan, Isabelle, Farris, Carol, Mitra, Siddhartha, Ramasamy, Gowthaman, Wang, Haiming, Tivey, Adrian, Jackson, Andrew, Houston, Robin, Parkhill, Julian, Holden, Matthew, Harb, Omar S., Brunk, Brian P., Myler, Peter J., Roos, David, Carrington, Mark, Smith, Deborah F., Hertz-Fowler, Christiane, and Berriman, Matthew

Published
2012
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47. TriTrypDB: a functional genomic resource for the Trypanosomatidae

Author

Aslett, Martin, Aurrecoechea, Cristina, Berriman, Matthew, Brestelli, John, Brunk, Brian P., Carrington, Mark, Depledge, Daniel P., Fischer, Steve, Gajria, Bindu, Gao, Xin, Gardner, Malcolm J., Gingle, Alan, Grant, Greg, Harb, Omar S., Heiges, Mark, Hertz-Fowler, Christiane, Houston, Robin, Innamorato, Frank, Iodice, John, Kissinger, Jessica C., Kraemer, Eileen, Li, Wei, Logan, Flora J., Miller, John A., Mitra, Siddhartha, Myler, Peter J., Nayak, Vishal, Pennington, Cary, Phan, Isabelle, Pinney, Deborah F., Ramasamy, Gowthaman, Rogers, Matthew B., Roos, David S., Ross, Chris, Sivam, Dhileep, Smith, Deborah F., Srinivasamoorthy, Ganesh, Stoeckert, Christian J., Jr, Subramanian, Sandhya, Thibodeau, Ryan, Tivey, Adrian, Treatman, Charles, Velarde, Giles, and Wang, Haiming

Published
2010
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49. Transmission of 'Candidatus Anaplasma camelii' to mice and rabbits by camel-specific keds, Hippobosca camelina.

Author

Bargul, Joel L., Kidambasi, Kevin O., Getahun, Merid N., Villinger, Jandouwe, Copeland, Robert S., Muema, Jackson M., Carrington, Mark, and Masiga, Daniel K.

Subjects
ANAPLASMA, TRYPANOSOMA, CANDIDATUS, RABBITS, CAMELINA, ZOONOSES
Abstract

Anaplasmosis, caused by infection with bacteria of the genus Anaplasma, is an important veterinary and zoonotic disease. Transmission by ticks has been characterized but little is known about non-tick vectors of livestock anaplasmosis. This study investigated the presence of Anaplasma spp. in camels in northern Kenya and whether the hematophagous camel ked, Hippobosca camelina, acts as a vector. Camels (n = 976) and > 10,000 keds were sampled over a three-year study period and the presence of Anaplasma species was determined by PCR-based assays targeting the Anaplasmataceae 16S rRNA gene. Camels were infected by a single species of Anaplasma, 'Candidatus Anaplasma camelii', with infection rates ranging from 63–78% during the dry (September 2017), wet (June-July 2018), and late wet seasons (July-August 2019). 10–29% of camel keds harbored 'Ca. Anaplasma camelii' acquired from infected camels during blood feeding. We determined that Anaplasma-positive camel keds could transmit 'Ca. Anaplasma camelii' to mice and rabbits via blood-feeding. We show competence in pathogen transmission and subsequent infection in mice and rabbits by microscopic observation in blood smears and by PCR. Transmission of 'Ca. Anaplasma camelii' to mice (8–47%) and rabbits (25%) occurred readily after ked bites. Hence, we demonstrate, for the first time, the potential of H. camelina as a vector of anaplasmosis. This key finding provides the rationale for establishing ked control programmes for improvement of livestock and human health. Author summary: Hematophagous flies such as Tabanids and Stomoxys, and other biting flies, are mechanical transmitters of various pathogens such as African trypanosomes and Anaplasma species. However, little is known about the role of common camel-specific biting keds (also known as camel flies or louse flies, genus Hippobosca) in pathogen transmission. Keds inflict painful bites to access host blood, and in the process may transmit bacterial hemopathogens. We demonstrated using amplicon sequencing that camel keds can transmit 'Candidatus Anaplasma camelii' from naturally-infected camels to healthy mice and rabbits via blood feeding. The high prevalence of camel anaplasmosis throughout the year in northern Kenya could be attributed to keds, which infest camels all year round. Unlike ticks, keds can fly from one host to another and thus promote disease transmission among and between camel herds. Although our study focused on the transmission of Anaplasma sp. by camel keds, these flies could possibly also transmit other hemopathogens through a similar mechanism. Notably, in the absence of their preferred hosts, keds occasionally bite humans and other vertebrates they come across in search of bloodmeals, and in the process could transmit zoonotic pathogens. [ABSTRACT FROM AUTHOR]

Published
2021
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