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Open AcceFocusHighlights of the XXI annual meeting of the Brazilian Society of Protozoology, the XXXII annual meeting on Basic Research in Chagas' disease & an international symposium on vesicle trafficking in parasitic Protozoa – 7 to 9 November 2005, Caxambu, Minas Gerais, BrazilJeffrey Shaw*†1, Sergio Schenkman†2 and Mauricio Martins Rodrigues†3

Address: 1Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Prof. Lineu Prestes, 1374, 05508-900 São Paulo, Brazil, 2Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, R. Botucatu 862 8A, 04023-062 São Paulo, Brazil and 3Departamento de Microbiologia, Imunologia e Parasitologia and Centro Interdisciplinar de Terapia Gênica (CINTERGEN), R. Mirassol, 207, 04044-010, São Paulo, Brazil

Email: Jeffrey Shaw* - jefreyj@usp.br; Sergio Schenkman - sergio@ecb.epm.br; Mauricio Martins Rodrigues - mrodrigues@ecb.epm.br

* Corresponding author †Equal contributors

AbstractThis report focuses on the 2005 Annual meeting held in Caxambu, Minas Gerais, Brazil that wasconvened and organized by the Brazilian Society of Protozoology http://www.sbpz.org.br/. This isan annual event and details of these meetings can be found on the Society's website. Within thespace available it has been impossible to cover all the important and fascinating contributions andwhat is presented are our personal views of the meetings scientific highlights and newdevelopments. The contents undoubtedly reflect each author's scientific interests and expertise.Fuller details of the round tables, seminars and posters can be consulted on line at http://www.sbpz.org.br/livroderesumos2005.php.

BackgroundThe meeting was attended by principally Brazilian scien-tists and students and a smaller number participants fromother Latin American countries, Europe, the United Statesand Japan. Of the 546 participants 72.94% (380) werestudents. The scientific sessions were divided into 10 peerlectures, 13 round tables in which 4 invited speakersexplored specific areas and 382 posters. There were also 4sessions in which selected posters were presented orally.In these sessions a total of 35 posters were presented bythe senior author who in most cases was a postgraduatestudent. In this report we provide a "snapshot" of what, inour view, are the highlights of newest developments.

The event was inaugurated by José Franco da Silveira (vicepresident of the Brazilian Society of Protozoology) whopresented an autobiographical sketch of the 2005 recipi-ent of the Samuel Pessoa award – Prof. Luiz HildebrandoPereira da Silva. Prof. Hildebrando, director of the "Insti-tuto de Pesquisas em Patologias Tropicais de Rondônia"(IPEPATRO), gave the opening Samuel Pessoa lectureemphasizing that parasitological research projects in aTropical Research Institute in Amazonia integrate scienceand regional health problems through collaborative pro-grams and "brain circulation". He highlighted the eco-nomic disequilibrium in Brazil caused by the destructionof the Amazonian forest by logging companies, cattle

Published: 17 August 2006

Kinetoplastid Biology and Disease 2006, 5:4 doi:10.1186/1475-9292-5-4

Received: 16 May 2006Accepted: 17 August 2006

This article is available from: http://www.kinetoplastids.com/content/5/1/4

© 2006 Shaw et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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farmers and soja bean planters. In spite of these productsbeing some of the countries principal exports they pro-duced an unacceptably low salary index per capita/peracre which could be higher if native forest resources wereexploited intelligently.

Cellular trafficMark Field (Cambridge University, UK) presented hisrecent data on the developmental regulation of endocyto-sis in Trypanosoma brucei, which undergoes massiveremodeling of its surface. He showed that bloodstreamand procyclics have different levels of small GTPases(Rabs) that control the traffic. Rab 11 is 20 fold enrichedin bloodstream compared to procyclic forms, while Rab 4levels are similar. Using RNAi his group demonstratedthat these two different stages have different patterns ofcellular traffic pathways and control and that over 600genes are involved in trafficking. But how is the regulationof genes orchestrated and what are mechanisms that con-trol the differential traffic during development? UlissesLopes from UFRJ showed that the Rho proteins ofTrypanosoma cruzi are small GTPases responsible forcytoskeleton remodeling mainly through actin filaments.One of them, TcRho1 presents a CaaX motif at the C-ter-minus that targets the protein for farnesylation. Mutantslacking the CaaX motif results in cell dispersion and deathduring differentiation, suggesting that is required for met-acyclogenesis. He also identified the OCRL1 and TcRJLs.The first is responsible for Lowe Syndrome in humans butits function in trypanosomes is unknown. The secondbelongs to a new family of Ras-related GTPase proteins inT. cruzi genome and is found in other trypanosomes andGiardia.

Using electron microscopy Maurilio Soare's group (UFRJ,Brazil) studied the endo and exocytic vesicles near theflagellar pocket of Trypanosoma cruzi and presented evi-dence of the presence of GM1 enriched lipid rafts in theseentry points. This type of membrane structure was alsodetected in the flagellum of T. brucei and T. cruzi by DavidEngman's group (Northwestern University, Chicago,USA). He showed that the flagellar calcium binding pro-tein (FCaBP) in these trypanosomes is dependent on myr-istoylation and palmitoylation, and calcium binding actsas a switch for the membrane localization. This is part ofa kinase signaling pathway that controls flagellar functionby affecting the lipid order and membrane organization.Lipid raftsstructures were also found by Narcisa Cunha eSilva's team (UFRJ, Brazil) in the reservosomes, which arelarge organelles present in T. cruzi epimastigotes that accu-mulate proteins and lipids. When the parasite undergoesmetacyclogenesis the reservosomes disappear.

The diversity and peculiarity of Rab small GTPase in vesic-ular trafficking of ameba was presented by Tomoyoshi

Nosaki (Gunna University Graduate School of Medicine,Japan). He compared phagocytosis of pathogenic Enta-moebae histolytica with non-pathogenic Entamoebae dispar.Amoeba phagosomes show small GTPases, Rab1/5/7/8and 11 in addition to several cytoskeleton components,signal transduction, transport, mitochondria-like protein,metabolic enzymes, ubiquitin systems and several hydro-lases (Euk. Cell and MBP 2005). Interestingly, amoebaehave a larger number (91) and unique Rab GTPase com-pared to humans or other higher eukaryotic cells (~60).Moreover, they have a unique pre-phagosomal vacuole(PPV), which contains protease and amoebapore that fuseto form primary and secondary phagosomes. Nosaki'sgroup characterized proteins interacting with Rab5 andRab7, involved in the formation of PPV.

Isabelle Coppens (John Hopkins University School ofPublic Health, USA) showed that Toxoplasma gondii usescellular trafficking to obtain host cell nutrients. The para-site manipulates the distribution of host cell microtubulesand vimentin but not actin to surround the parasitopho-rous vacuole (PV) in a way that a corset of host microtu-bules is formed around it. This dynamic association isused to divert low-density lipoproteins (LDL). One com-ponents of this machinery is GRA7, a 236 amino acid pro-tein, which acts like a garrote that sequesters hostendocytic organelles within the vacuolar space. My-HangHuynh's team (John Hopkins University, USA), presentedaspects of trafficking involved in T. gondii cell invasion inwhich proteins found in micronemes are secreted to formthe new PV. By knocking-out T. gondii M2AP protein, theyfound a decrease in the microneme MIC2 expression,which is retained in the ER/Golgi, severe impairment ofcell invasion in vitro, attenuated virulence as well as glid-ing motility problems. They propose as a model in whichM2AP forms a complex with MIC2 in an early endosome,which is processed and added to micronemes.

Host parasite interactionOscar N. Mesquita (UFMG, Brazil) examined membranealterations during the interaction of macrophages withLeishmania by defocusing under optical microscopy. Hedetected and quantified small random changes and largealterations as ruffles on the cell surface. The variationswere conserved, indicating that they are produced by dis-crete events. Ruffles were inhibited by adding cytochala-sin. When a parasite is added to the cell using the opticaltweezers he found dramatic perturbations in the smallmovements, but ruffling activity was not modified. Anto-nio Gonzalez Aguilar (CSIP, Spain) demonstrated that thealternative splice of the Lyt1 gene of T. cruzi generates amembrane protein. This membrane protein is the TcToxinvolved in the parasite's escape from the PV. Phytomonasserpens that expresses this gene is able to escape from thePV and multiply in the macrophage's cytoplasm. The

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other spliced form of Lyt1, codes for a protein expressedin the epimastigote's kinetoplast, and is probablyinvolved in DNA replication.

Control of gene expressionArtur Scherf (Institute Pasteur, France) described recentadvances in explaining the expression of Var genes by Plas-modium falciparum. Var genes encode the Plasmodiumerythrocyte surface proteins (Pefr1), whose expressiondelimits infected red cell adhesion. Dr Scherf proposed amodel for the control of Car gene expression that dependson where the Var gene is located in the nucleus. Non-expressed Var genes are in heterochromatin regions thatprevents transcription. In contrast, the expressed Var genechromatin is acetylated outside the heterochromaticregion. The next question to be answered is how the gene'sexpression site is selected?

T. cruzi surface mucin-like molecules are encoded by alarge multigene family. Vanina Campo (Instituto deInvestiagaciones Biotecnológicas, Argentina), explainedthat the expression of this diverse group of genes is con-trolled by post-transcriptional mechanism, includingalternative splicing and mRNA stabilization. Key factorsthat control expression are RNA recognition motives inthese genes, which are sites for binding of protein factorsthat stabilize specifically groups of mRNA. Stenio Fragoso(IBMP, Brazil) characterized TcZFP1a CCH-zinc fingerprotein, possibly involved in post-translation control ofgene expression. He showed that it is expressed cells sub-mitted to nutritional stress and is located in cytoplasmicspots. The protein expressed in E. coli in fusion with GFPand purified by Ni-columns interacts with RNA sequencescontaining poly C RNA. It does not bind to AU rich ele-ments (ARE). This, together with other CCH zinc fingerproteins, is differentially expressed during metacyclogen-esis as seen by microarray analysis.

T. cruzi is composed by two major phylogenetic groups, T.cruzi I and T. cruzi II. Santuza Teixeira's group (UFMG,Brazil) found that multigene families of group I are morehomogeneous than those of group II. Hybrid strainsshowed intermediate variability. According to her data,mismatch excision repair may be different in the twogroups, particularly TcMSH2 activity, one of the proteinsresponsible for this type of repair. Nancy Sturm (UCLA,USA) showed polymorphisms in the kinetoplast maxicir-cle sequences of these two groups and that a variable RNAediting could compensate these differences.

A key factor in explaining differential gene expression oftrypanosomatids is the control of translation initiation.The group lead by Oswaldo Pumpilio Melo Neto(FIOCRUZ, Brazil) presented results characterizing multi-ple homologues for the eIF4E subunits of Leishmania and

Trypanosoma involved in cap binding and translation ini-tiation control in trypanosomes. L. major has four homo-logues but only eIF4E1 binds to cap, while in T. bruceiboth eIF4E1 and E2 are involved in this same process butthat, only eIF4E3 was essential.

EpidemiologyThe Sudan is one of the countries that has had some of theworst epidemics of visceral leishmaniasis (VL) known toman and Muntaser Irahim (Institute of Endemic Diseases,Sudan) compared this disease to a serial killer. The actualnumber of people who have died over the years isunknown but when the epidemic in the West Nile regionwas first recorded in the 1950's a whole tribe died waswiped out. Since then there have been estimates that over250,000 people have been victims of the "serial killer".The variable severity of the disease is considered to belinked to both ethnic and geographical elements. Recentlyit has been shown that the graver symptoms leading todeath are linked to certain genes. In Brazil it has beennoted that VL epidemics have a 10 year cycle and it was asurprise to learn that in the Sudan the disease also strikesevery ten years. Detailed molecular studies have shownthat the aetiological agent, Leishmania (Leishmania)archibaldi is closer to L.(L.) donovani and it has been sug-gested that the latter originated from the former whenman migrated from Africa. There is a possibility that thereare wild animal reservoirs and that these are in fact the pri-mary source, however, in its epidemic form the disease isclearly an anthroponosis.

Highlights of immunologyDiverse aspects of immunity and immunopathology ofmalaria, leishmaniasis, Chagas' disease and toxoplasmo-sis were addressed.

The malaria speakers enriched our knowledge on diversetopics such as the molecular aspects of the immunopa-thology of P. falciparum malaria and the presence of cross-reactive epitopes between diverse species of malaria para-sites. Jürg Gysin (Institut Pasteur, France) described hiswork on a roptry protein (RSP-2) which is present on thesurface of non-infected human erythrocytes. His resultssuggest that in part anemia is related to the destruction ofthese cells by RSP-2 specific antibodies with the aid ofmonocytes. Subsequently, Lars Hviid (Rigshospitalet,Denmark) summarized several years of studies on preg-nancy-associated malaria (PAM) which established thatPAM resulted from preferential sequestration of parasit-ized red blood in the placenta. The molecular target forimmunity against PAM was identified as the PfEMP-1(var2CSAgene) which is expressed on the surface ofinfected red blood cells capable of binding to chondroitinsulfate A. Based on this they proposed an anti-PAM vac-cine. Gerhard Wunderlich (USP, Brazil) concluded that

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the repertoire of the P. falciparum var genes in the AmazonBasin is limited and that this indicated a reduced genepool of this species throughout the region. Denise Mattei(Institute Pasteur, France) elucidated some of the mecha-nism by which clag-2 gene products modulates adhesionof infected red blood cells through expression of certainPfEMP-1. Finally, Antoniana Krettli (FIOCRUZ, Brazil)discussed the presence of cross-reactive epitopes presentin sporozooites of P. falciparum and P. gallinaceum sporo-zooites. This cross-reactive epitope may be a new anti-genic marker for the detection of protective immunityagainst P. falciparum sporozooites.

Flavia Ribeiro-Gomez (UFRJ, Brazil) found that the courseof experimental infection with L. major can be modifiedby the presence of apoptotic neutrophils. In the case ofBALB/c mice these cells have a deleterious role in theinfection mediated by the increase in secretion of TGF-beta by macrophages. On the other hand, the presences ofapoptotic neutrophils increase the resistance of C57BL/6mice by a mechanism that is dependent on the neutrophilelastase, and TNF-alpha and NO secretion.

The presentations on the immunity to T. cruzi focused onsubjects that are expected to be the new trends in the yearsto come. Sarah Williams-Blangero (South-Western Foun-dation for Biomedical Research, USA) described eleganthuman genetic studies concluding that several clinical fea-tures of chronic Chagas' disease are genetically linked.Nobuko Yoshida (UNIFESP, Brazil) shed some light onthe poorly understood molecular mechanisms responsi-ble for oral infection, describing also a possible methodfor the eventual blockage of this type of infection. Mau-rico Rodrigues (UNIFESP, Brazil) focused his presentationon a so far poorly studied molecule extremely abundantin the amastigote forms of the parasite. He concluded thatthe amastigote surface protein-2 is highly conservedamong the different strains of the parasite being recog-nized by protective CD4 Th1 and CD8 Tc1 cells. Theseresults indicate that this molecule may provide an excel-lent target for vaccination. Walderez Dutra (UFMG, Bra-zil) explored the presence of regulatory molecules on thesurface of antigen presenting cells (APC) as key factorscontrolling the reactivity of pathogenic T lymphocytes. Sofar, she has observed that APC from symptomatic individ-uals have an activated profile that may explain at least inpart the higher reactivity of T lymphocytes. Studies inChagasic humans performed by Juliana de Assis(FIOCRUZ, Brazil) described an interesting correlationbetween the frequency of CD4+CD25+ regulatory cellsand the indeterminate forms of the disease. Joseli Lannes(FIOCRUZ, Brazil) presented data where she describedthat CCR5 inhibitors may be explored as tools to reducethe heart immunopathology of experimental Chagas' Dis-ease.

Monoxenic TrypanosomatidsThe presentations at round table on the monoxenics andevolutionary perspectives of the Trypanosomatidae familyranged from the origin of endosymbionts to origin of thegroup. Cristina Motta (UFRJ, Brasil) emphasized that thetrypanosomatid endosymbiont cannot survive outside itshost and that like mitochondria it lacks the septum andFtsZ ring that are essential in bacterial division. Recentsequence data indicates that they are closely related to Bor-detella bronchiseptica and that endosymbiosis was a singleevent. Based on the 18S rRNA, SL RNA and protein codinggenes from an extensive taxa set Julius Lukes (Institute ofParasitology, Czech Republic) concluded the trypano-somatids were monophyletic group that originated fromparaphyletic bodonids. The 18S rRNA was not informa-tive for insect parasites and indicated that members of thisgroup are not host specific. Similarly bird trypanosomesdo not appear to be vector specific and are found in mos-quitoes, black flies, hippoboscids and midges. The vectorof the T. avium clade in the Czech Republic appears to beblack flies while the United Kingdom the vectors of the T.corvi clade are hippoboscids and mosquitoes. Thereappears to be an overall low level of host specificity withthe surprising possibility of insect parasites infectingwarm blooded vertebrates. The available taxonomic datastrongly favours the hypothesis that the group evolvedfrom flagellates of insects. One of the important biologi-cal characters of the trypanosomatids is that their mor-phology is reversible during their life cycles and AngelaLopes (UFRJ) questioned what mechanisms are responsi-ble for this cellular modulation. She drew attention topotential importance of platelet-activating factor (PAF) inthis process. PAF is a phosopholipid with that has diversephysiological and patho-physiological actions. Anothersubstance found in serum and reduviid bug saliva, lyso-phosphatidycholine (LPC) has been found to modulatecellular differentiation of Herpetosoma samuelpessoai and itis possible that LPC reacts via the PAF receptor. There hasbeen an increase in immuno-suppressed individuals inrecent years and human cases of monoxenic trypano-somatids in man have been recorded. With this in mindElvira Saraiva (UFRJ, Brazil) investigated the infectivity ofBlastocrithidia culcis to human monocytes that had beenexposed to HIV-1 transactivator protein. The intracellularsurvival of B. culcis was greater in cells exposed to HIV-1Tat protein and TGF-β1. In Aedes aegypti the parasiteadhered and penetrated the gut wall and adhered to thesalivary gland wall. This could lead to transmission by bitewhich could lead to infection in immuno-suppressedindividuals.

Chemotherapy & treatmentThe problems of developing new drugs for neglected dis-eases were discussed by Simon Croft, coordinator ofDrugs for Neglected Diseases initiative (DNDi – http://

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www.dndi.org). The development cost of a new drug is inthe order of US$800 million dollars which is prohibitivefor neglected diseases such as malaria and tuberculosis.He emphasized that there have been enormous advancesin biochemical and cell biological studies of the patho-gens such as leishmania and trypanosomes but that thedata must be used in an organized fashion for theResearch and Development (R & D) of new drugs. Themajor R & D stumbling block in the past has been the lackof coordinated efforts between commercial companieswho have the expertise and groups from the countries inwhich the diseases are endemic. However this is possiblewith sustainable funding and to this end non profit mak-ing organizations have been formed to funnel funds intothis area and forge collaborative links. A virtual model tar-geting the product profile has been developed to accom-pany development at different stages so that decisions asto the feasibility of success can be critically assessed, thusavoiding investing in a product that will not meet thebasic requirements.

Other participants discussed the specific need for thedevelopment of drugs for leishmaniasis and Americantrypanosomiasis. Eder Romero (Universidade Nacionalde Quilmes, Argentina) explored the use of nanotechnol-ogy for delivering drugs in concentrations up to 100 timesless than those administered by traditional methods. Thedelivery vehicle (nanoship) also has the advantage ofbeing able to target a specific disease compartment ateither the tissue or cellular level. Federico Gomes-de-las-Herus, (GlaxoSmithkline disease of the developing WorldDrug Discovery Centre, Spain) explained how the GSKcentre, which has 100 full time scientists and the full sup-port of the parent drug company, works via a partnershipwith Medicines for Malarial Venture (MMV) and GlobalAlliance for TB (GATB) in developing new drugs formalaria and tuberculosis. An important concept in thisprocess is the Target Product Profile which for malaria is:treatment of uncomplicated malaria, suitable for sensitive& resistant Plasmodium, oral administration and fast activ-ity, 3 day treatment, well tolerated, suitable for use incombinations and affordable for the target population. Itwas emphasized that the high cost of drugs is because veryfew reach the market place. Hector Freilij (Hospital deNiños Ricardo Gutiérez, Argentina) drew attention to theimportance of congenital transmission of Chagas diseasein urban areas of large towns such as Buenos Aires. Theinfected mothers are from endemic areas and are asymp-tomatic. Of three children only one may become infectedduring pregnancy and treatment of the children under 5years old is successful. In urban areas of Argentina Chagasdisease has become a childhood disease and the majorityof the children are asymptomatic. A major question is ifsuch cases go untreated will they develop the more severeclinical forms of Chagas disease later in their lives. Luis

Villa Villanueva (Médecins San Frontiéres, Spain) voicedhis concern as to the availability of drugs for the treatmentof Chagas Disease since the major drug companies werenot interested in continuing to manufacture them. Alter-native manufacturing sources within endemic countriesare a solution to this problem and Biomaguinhos(FIOCRUZ, Brazil) has signed contracts to produce some.It was pointed out that this may solve Brazil's future prob-lem but will it help other Latin American countries whereChagas disease is endemic?

The treatment of the extreme variety of clinical forms ofcutaneous leishmaniasis that may lead to more severeclinical symptoms such as mucocutaneous leishmaniasisand diffuse cutaneous leishmaniasis is a challenge to theclinician. Edgar de Carvalho (UFB, Brasil) addressed thisproblem by documenting some of the important immu-nological parameters (IFN-γ, TNF-α, IL2, IL-10 IL15, andT cells CD4, CD8, CD69, CD28-, CD62L-) associated withthe different clinical forms. With the intuitive of improv-ing the chemotherapeutic responses GM-CSF and pentox-yfilline were associated with antimony therapy to controlsome of the adverse effects caused by the cytokines.

Parasite vector interactionMarcelo Jacobs-Lorena (Malaria Research Institute, USA)reviewed the approach of using transgenic mosquitoes inpreventing malaria transmission. The main strategy hasbeen to genetically engineer mosquitoes to make themresistant to the pathogen, introduce them into the popu-lation that will theoretically reduce transmission. Hestressed that this is a complementary approach to drugsand vaccines. Due to the complexity of the fitness prob-lem in the nature, his group is now trying to introducetransformed bacteria as a source of heterologous genes(paratransgenic). He also showed his recent resultsdescribing the role of SPRN6, a member of the serine pro-tease inhibitor (serpin) family, which is expressed byinsect infected cells. SPRN6 RNAi and knockouts have anincreased infection load. More interesting is the fact thatexpression of this protein is differently involved in themosquitos' defenses against different species of Plasmo-dium. In another presentation, Eloi Garcia (FIOCRUZ,Brazil) reported the role of eicosanoids in trypanosoma-tid-triatomine interactions. He focused his talk on theinteraction of Rhodnius prolixus with Trypanosoma rangeli.The vector is infected when it feeds; the parasite prolifer-ates in the gut and is eliminated with faeces but in approx-imately 10% of the insects the flagellates penetrate the gutwall and reach the salivary gland. Data published in 2004showed that eicosanoids produced by insect cells protectthe vector against T. rangeli induced mortality. Theincrease in mortality is correlated with decrease in aggre-gation of hemocytes, the defense cells that are present inthe insect hemolymph. In contrast, hemocyte microaggre-

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gation is promoted by arachidonic acid, which protectsthe insects. Possible platelet-activating factor (PAF) likemolecules are being proposed to mediate these aggrega-tion effects since the WEB 2086, a PAF agonist, increasedinsect survival, at the same time that less hemocytes aggre-gation was seen.

The meeting's closing conference was given by AntonioTeixeira (UnB, Brazil) who discussed the pathology ofChagas Disease and evidence that T. cruzi is in fact thegenetic vector of kinetoplast DNA. The integration of par-asite kDNA into the vertebrate genome in this scenariowould be responsible for the immunopathology of Cha-gas' disease.

Competing interestsThe author(s) declare that they have no competing inter-ests.

Authors' contributionsAll authors contributed equally to the preparation of thisreport.

AcknowledgementsThe authors would like to publicly thank the Brazilian Research Council (CNPq), the São Paulo State Foundation for the Support of Research (FAPESP), the Minas Gerais State Foundation for the Support of Research (FAPEMIG) and the Oswaldo Cruz Institute Foundation (FIOCRUZ), the Rio de Janeiro State Foundation for the Support of Research (FAPERJ), the Foundation for Training in Higher Education (CAPES) who for many years have collectively supported the Caxambu meetings.

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