Participation of Trypanosoma cruzi gp63 molecules on the interaction with Rhodnius prolixus

AbstractTrypanosoma cruzi is the causative agent of Chagas disease, a vector-borne disease. The parasite molecules involved in vector interaction have been little investigated. Metallopeptidases and gp63 molecules have been implicated in parasite adhesion of several trypanosomatids to the insect midgut. Although gp63 homologues are highly expanded in the T. cruzi genome, and are implicated in parasite–mammalian host interaction, its role in the insect vector has never been explored. Here, we showed that divalent metal chelators or anti-Tcgp63-I antibodies impaired T. cruzi adhesion to Rhodnius prolixus midgut. Parasites isolated after insect colonization presented a drastic enhancement in the expression of Tcgp63-I. These data highlight, for the first time, that Tcgp63-I and Zn-dependent enzymes contribute to the interaction of T. cruzi with the insect vector.

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Trypanosoma cruzi heparin-binding proteins mediate the adherence of epimastigotes to the midgut epithelial cells of Rhodnius prolixus

Parasitology ◽

10.1017/s0031182011002344 ◽

2012 ◽

Vol 139 (6) ◽

pp. 735-743 ◽

Cited By ~ 16

Author(s):

F. O. R. OLIVEIRA ◽

C. R. ALVES ◽

F. SOUZA-SILVA ◽

C. M. CALVET ◽

L. M. C. CÔRTES ◽

...

Keyword(s):

Epithelial Cells ◽

Trypanosoma Cruzi ◽

Mammalian Cells ◽

Binding Proteins ◽

Rhodnius Prolixus ◽

Insect Vector ◽

Heparin Binding ◽

Molecular Masses ◽

Pre Treatment

SUMMARYHeparin-binding proteins (HBPs) have been demonstrated in both infective forms of Trypanosoma cruzi and are involved in the recognition and invasion of mammalian cells. In this study, we evaluated the potential biological function of these proteins during the parasite-vector interaction. HBPs, with molecular masses of 65·8 kDa and 59 kDa, were isolated from epimastigotes by heparin affinity chromatography and identified by biotin-conjugated sulfated glycosaminoglycans (GAGs). Surface plasmon resonance biosensor analysis demonstrated stable receptor-ligand binding based on the association and dissociation values. Pre-incubation of epimastigotes with GAGs led to an inhibition of parasite binding to immobilized heparin. Competition assays were performed to evaluate the role of the HBP-GAG interaction in the recognition and adhesion of epimastigotes to midgut epithelial cells of Rhodnius prolixus. Epithelial cells pre-incubated with HBPs yielded a 3·8-fold inhibition in the adhesion of epimastigotes. The pre-treatment of epimastigotes with heparin, heparan sulfate and chondroitin sulfate significantly inhibited parasite adhesion to midgut epithelial cells, which was confirmed by scanning electron microscopy. We provide evidence that heparin-binding proteins are found on the surface of T. cruzi epimastigotes and demonstrate their key role in the recognition of sulfated GAGs on the surface of midgut epithelial cells of the insect vector.

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Induction of Trypanosoma cruzi Metacyclogenesis in the Gut of the Hematophagous Insect Vector, Rhodnius prolixus, by Hemoglobin and Peptides Carrying αD-Globin Sequences

Experimental Parasitology ◽

10.1006/expr.1995.1116 ◽

1995 ◽

Vol 81 (3) ◽

pp. 255-261 ◽

Cited By ~ 47

Author(s):

E.S. Garcia ◽

M.S. Gonzalez ◽

P. Deazambuja ◽

F.E. Baralle ◽

D. Fraidenraich ◽

...

Keyword(s):

Trypanosoma Cruzi ◽

Rhodnius Prolixus ◽

Insect Vector ◽

Hematophagous Insect

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Tenuivirususes a molecular bridge strategy to overcome insect midgut barriers for virus persistent transmission

10.1101/404657 ◽

2018 ◽

Author(s):

Gang Lu ◽

Shuo Li ◽

Changwei Zhou ◽

Xin Qian ◽

Qing Xiang ◽

...

Keyword(s):

Brown Planthopper ◽

Specific Interaction ◽

Virus Transmission ◽

Plant Viruses ◽

Insect Vector ◽

Terminal Protein ◽

Insect Midgut ◽

Helper Component ◽

Vector Interaction ◽

Molecular Bridge

AbstractMany persistent transmitted plant viruses, includingRice stripe tenuivirus(RSV), cause serious damages to crop productions in China and worldwide. Although many reports have indicated that successful insect-mediated virus transmission depends on proper virus–insect vector interactions, the mechanism(s) controlling interactions between viruses and insect vectors for virus persistent transmission remained poorly understood. In this study, we used RSV and its small brown planthopper (SBPH) vector as a working model to elucidate the molecular mechanism controlling RSV virion entrance into SBPH midgut for persistent transmission. We have now demonstrated that this non-envelopedTenuivirususes its non-structural glycoprotein NSvc2 as a helper component to bridge the specific interaction between virion and SBPH midgut cells, leading to overcome SBPH midgut barriers for virus persistent transmission. In the absence of this glycoprotein, purified RSV virion is not capable of entering SBPH midgut cells. In RSV-infected cells, glycoprotein NSvc2 is processed into two mature proteins: an amino-terminal protein NSvc2-N and a carboxyl-terminal protein NSvc2-C. We determined that NSvc2-N interacted with RSV virion and bound directly to midgut lumen surface via its N-glycosylation sites. Upon recognition by midgut cells, the midgut cells underwent endocytosis followed by compartmentalizing RSV virion and NSvc2 into early and then late endosomes. The acidic condition inside the late endosome triggered conformation change of NSvc2-C and caused cell membrane fusion via its highly conserved fusion loop motifs, leading to the release of RSV virion from endosome into cytosol. In summary, our results showed for the first time that a riceTenuivirususes a molecular bridge strategy to ensure proper interactions between virus and insect midgut for successful persistent transmission.Author summaryOver 75% of the known plant viruses are insect transmitted. Understanding how plant viruses interacted with their insect vectors during virus transmission is one of the key steps to manage virus diseases worldwide. Both the direct and indirect virus–insect vector interaction models have been proposed for virus non-persistent and semi-persistent transmission. However, the indirect virus–vector interaction mechanism during virus persistent transmission has not been reported previously. In this study, we developed a new reverse genetics technology and demonstrated that the circulative and propagative transmittedRice stripe tenuivirusutilizes a glycoprotein NSvc2 as a helper component to ensure a specific interaction betweenTenuivirusvirion and midgut cells of small brown planthopper (SBPH), leading to conquering the midgut barrier of SBPH. This is the first report of a helper component mediated-molecular bridge mechanism for virus persistent transmission. These new findings and our new model on persistent transmission expand our understanding of molecular mechanism(s) controlling virus–insect vector interactions during virus transmission in nature.

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Trypanosoma cruzi-infected Rhodnius prolixus endure increased predation facilitating parasite transmission to mammal hosts

PLoS Neglected Tropical Diseases ◽

10.1371/journal.pntd.0009570 ◽

2021 ◽

Vol 15 (7) ◽

pp. e0009570

Author(s):

Newmar Pinto Marliére ◽

Marcelo Gustavo Lorenzo ◽

Alessandra Aparecida Guarneri

Keyword(s):

Trypanosoma Cruzi ◽

Effective Means ◽

Rhodnius Prolixus ◽

Parasite Transmission ◽

Intermediate Hosts ◽

Oral Transmission ◽

Vector Interaction ◽

Triatomine Bugs ◽

Increased Risk ◽

Predation Rates

Triatomine bugs aggregate with conspecifics inside shelters during daylight hours. At dusk, they leave their refuges searching for hosts on which to blood feed. After finding a host, triatomines face the threat of being killed, because hosts often prey on them. As it is known that many parasites induce the predation of intermediate hosts to promote transmission, and that ingestion of Trypanosoma cruzi-infected bugs represents a very effective means for mammal infection, we hypothesized that trypanosomes induce infected bugs to take increased risk, and, as a consequence, be predated when approaching a host. Therefore, we evaluated whether the predation risk and predation rates endured by Rhodnius prolixus increase when infected with T. cruzi. Assays were performed in square glass arenas offering one central refuge to infected and uninfected 5th instar nymphs. A caged mouse was introduced in each arena after a three-day acclimation interval to activate sheltered insects and induce them to approach it. As hypothesized, a significantly higher proportion of infected insects was predated when compared with uninfected ones (36% and 19%, respectively). Indeed, T. cruzi-infected bugs took higher risk (Approximation Index = 0.642) when compared with healthy ones (Approximation Index = 0.302) and remained outside the shelters when the host was removed from the arena. Our results show that infection by T. cruzi induces bugs to assume higher risk and endure higher predation rates. We reveal a hitherto unknown trypanosome-vector interaction process that increases infected bug predation, promoting increased rates of robust oral transmission. The significant consequences of the mechanism revealed here make it a fundamental component for the resilient maintenance of sylvatic, peridomestic and domestic cycles.

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First finding of Trypanosoma cruzi II in vampire bats from a district free of domestic vector-borne transmission in Northeastern Argentina

Parasitology ◽

10.1017/s0031182016000925 ◽

2016 ◽

Vol 143 (11) ◽

pp. 1358-1368 ◽

Cited By ~ 8

Author(s):

HERNÁN D. ARGIBAY ◽

M. MARCELA OROZCO ◽

M. VICTORIA CARDINAL ◽

MIGUEL A. RINAS ◽

MARÍA ARNAIZ ◽

...

Keyword(s):

Trypanosoma Cruzi ◽

Pcr Amplification ◽

Variable Region ◽

Wild Mammals ◽

Vampire Bats ◽

Vector Borne ◽

Transmission Cycles ◽

First Time ◽

Dna Pcr ◽

Northeastern Argentina

SUMMARYEstablishing the putative links between sylvatic and domestic transmission cycles of Trypanosoma cruzi, the etiological agent of Chagas disease, is of public health relevance. We conducted three surveys to assess T. cruzi infection in wild mammals from a rural and a preserved area in Misiones Province, Northeastern Argentina, which had recently been declared free of vector- and blood-borne transmission of human T. cruzi infection. A total of 200 wild mammals were examined by xenodiagnosis (XD) and/or polymerase chain reaction (PCR) amplification of the hyper-variable region of kinetoplast DNA minicircles of T. cruzi (kDNA-PCR). The overall prevalence of T. cruzi infection was 8%. Nine (16%) of 57 Didelphis albiventris opossums and two (7%) of 29 Desmodus rotundus vampire bats were positive by both XD and kDNA-PCR. Additionally, one D. rotundus positive for T. cruzi by kDNA-PCR tested positive by satellite-DNA-PCR (SAT-DNA-PCR). The T. cruzi-infected bats were captured indoors and in the yard of a vacant dwelling. All D. albiventris were infected with TcI and both XD-positive D. rotundus by TcII. Fifty-five opossum cubs within the marsupium were negative by XD. The mean infectiousness to the vector was 62% in D. albiventris and 50% in D. rotundus. Mice experimentally infected with a parasite isolate from a vampire bat displayed lesions typically caused by T. cruzi. Our study documents the presence of the genotype TcII in a sylvatic host for the first time in Argentina, and the occurrence of two transmission cycles of T. cruzi in a district free of domestic vector-borne transmission.

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Neolignans inhibit Trypanosoma cruzi infection of its triatomine insect vector, Rhodnius prolixus

Parasitology Research ◽

10.1007/s004360050532 ◽

1999 ◽

Vol 85 (3) ◽

pp. 184-187 ◽

Cited By ~ 13

Author(s):

Marise M. O. Cabral ◽

Patrícia Azambuja ◽

Otto R. Gottlieb ◽

Eloi S. Garcia

Keyword(s):

Trypanosoma Cruzi ◽

Rhodnius Prolixus ◽

Insect Vector ◽

Cruzi Infection

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Towards an understanding of the interactions of Trypanosoma cruzi and Trypanosoma rangeli within the reduviid insect host Rhodnius prolixus

Anais da Academia Brasileira de Ciências ◽

10.1590/s0001-37652005000300004 ◽

2005 ◽

Vol 77 (3) ◽

pp. 397-404 ◽

Cited By ~ 51

Author(s):

Patrícia Azambuja ◽

Norman A. Ratcliffe ◽

Eloi S. Garcia

Keyword(s):

Trypanosoma Cruzi ◽

Developmental Stages ◽

Rhodnius Prolixus ◽

Parasite Development ◽

Insect Vector ◽

Defense System ◽

Parasite Strain ◽

Trypanosoma Rangeli ◽

Physiological Processes ◽

Prophenoloxidase System

This review outlines aspects on the developmental stages of Trypanosoma cruzi and Trypanosoma rangeli in the invertebrate host, Rhodnius prolixus. Special attention is given to the interactions of these parasites with gut and hemolymph molecules and the effects of the organization of midgut epithelial cells on the parasite development. The vector insect's permissiveness to T. cruzi, which develops in the vector gut, largely depends on the host nutritional state, the parasite strain and the molecular interactions with trypanolytic compounds, lectins and resident bacteria in the gut. T. rangeli invades the hemocoel and once in the hemolymph, can be recognized and activates the defense system of its insect vector, i.e., the prophenoloxidase system, phagocytosis, hemocyte microaggregation, superoxide and nitric oxide activity and the eicosanoid biosynthesis pathway. Taken together, these findings not only provide a better understanding of the interactions parasite - insect vector, but also offer new insights into basic physiological processes involved in the parasites transmission.

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Involvement of sulfated glycosaminoglycans on the development and attachment of Trypanosoma cruzi to the luminal midgut surface in the vector, Rhodnius prolixus

Parasitology ◽

10.1017/s0031182011001521 ◽

2011 ◽

Vol 138 (14) ◽

pp. 1870-1877 ◽

Cited By ~ 8

Author(s):

MARCELO S. GONZALEZ ◽

LUIZ-CLAUDIO F. SILVA ◽

J. M. ALBUQUERQUE-CUNHA ◽

NADIR F. S. NOGUEIRA ◽

DÉBORA P. MATTOS ◽

...

Keyword(s):

Epithelial Cells ◽

Rhodnius Prolixus ◽

Parasite Infection ◽

Insect Vector ◽

Luminal Surface ◽

Anionic Sites ◽

Insect Midgut ◽

Posterior Midgut

SUMMARYIn the present study, we investigated the involvement of sulfated glycosaminoglycans in both the in vivo development and adhesion of T. cruzi epimastigotes to the luminal surface of the digestive tract of the insect vector, Rhodnius prolixus. Pre-incubation of T. cruzi, Dm 28c epimastigotes with heparin, chondroitin 4-sulfate, chondroitin 6-sulfate or protamine chloridrate inhibited in vitro attachment of parasites to the insect midgut. Enzymatic removal of heparan sulfate moieties by heparinase I or of chondroitin sulfate moieties by chondroitinase AC from the insect posterior midgut abolished epimastigote attachment in vitro. These treatments also reduced the labelling of anionic sites exposed at the luminal surface of the perimicrovillar membranes in the triatomine midgut epithelial cells. Inclusion of chondroitin 4-sulfate or chondroitin 6-sulfate and to a lesser extent, heparin, in the T. cruzi-infected bloodmeal inhibited the establishment of parasites in R. prolixus. These observations indicate that sulfated glycosaminoglycans are one of the determinants for both adhesion of the T. cruzi epimastigotes to the posterior midgut epithelial cells of the triatomine and the parasite infection in the insect vector, R. prolixus.

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Amastigotes of Trypanosoma cruzi escape destruction by the terminal complement components.

Journal of Experimental Medicine ◽

10.1084/jem.169.3.881 ◽

1989 ◽

Vol 169 (3) ◽

pp. 881-891 ◽

Cited By ~ 36

Author(s):

K Iida ◽

M B Whitlow ◽

V Nussenzweig

Keyword(s):

Trypanosoma Cruzi ◽

Alternative Pathway ◽

Surface Protein ◽

Protozoan Parasite ◽

Mammalian Host ◽

Insect Vector ◽

Complement Components ◽

Life Cycle Stages ◽

Sds Page ◽

Terminal Complement

We studied the effect of complement on two life cycle stages of the protozoan parasite Trypanosoma cruzi: epimastigotes, found in the insect vector, and amastigotes, found in the mammalian host. We found that while both stages activate vigorously the alternative pathway, only epimastigotes are destroyed. The amounts of C3 and C5b-7 deposited on the amastigotes were similar to those bound to the much larger epimastigotes. Binding of C9 to amastigotes was four to six times less than binding to epimastigotes, resulting in a lower C9/C5b-7 ratio. Although a fairly large amount of C9 bound stably to amastigotes, no functional channels were formed as measured by release of incorporated 86Rb. The bound C9 had the characteristic properties of poly-C9, that is, it expressed a neo-antigen unique to poly-C9, and migrated in SDS-PAGE with an apparent Mr greater than 10(5). The poly-C9 was removed from the surface of amastigotes by treatment with trypsin, indicating that it was not inserted in the lipid bilayer. Modification of amastigote surface by pronase treatment rendered the parasites susceptible to complement attack. These results suggest that amastigotes have a surface protein that binds to the C5b-9 complex and inhibits membrane insertion, thus protecting the parasites from complement-mediated lysis.

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Kindling, Logs, and Coals: The Dynamics of Trypanosoma cruzi, the Etiological Agent of Chagas Disease in Arequipa, Peru

Population Biology of Vector-Borne Diseases ◽

10.1093/oso/9780198853244.003.0012 ◽

2020 ◽

pp. 215-226

Author(s):

Michael Z. Levy

Keyword(s):

Trypanosoma Cruzi ◽

Salivary Glands ◽

Chagas Disease ◽

Etiologic Agent ◽

Etiological Agent ◽

Insect Vector ◽

Blood Sucking ◽

Vector Borne ◽

Triatomine Insects

The forces that lead to the emergence of Trypanosoma cruzi, the etiologic agent of Chagas disease, are often distinct from those that maintain its transmission, and these are distinct again from those that allow the parasite to persist over decades. Just as kindling, logs, and coals all play discrete roles in the growth of a fire, a myriad of mammalian hosts contribute differently to epidemics of Trypanosoma. cruzi. Chagas disease affects millions of people in the Americas, and, through migration, thousands more on other continents. The agent of the disease, Trypanosoma cruzi, is a slender, highly-motile, unicellular parasite. T. cruzi does not migrate to the salivary glands of its insect vector–the blood-sucking triatomine insects–as many other vector-borne parasites do.

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