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Pathogens
Special Issues
Virulence and Molecular Cell Biology of Parasites
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Virulence and Molecular Cell Biology of Parasites

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Parasitic Pathogens".

Deadline for manuscript submissions: 20 March 2026 | Viewed by 2409

Special Issue Editor

Prof. Dr. Jorge González

E-Mail Website
Guest Editor
Laboratorio de Parasitología Molecular, Departamento de Tecnología Médica, Facultad de Ciencias de la Salud, Universidad de Antofagasta, Antofagasta 1270300, CP, Chile
Interests: Trypanosoma cruzi; virulence; signal transductions; proteomics

Special Issue Information

Dear Colleagues,

Over millions of years, parasites have been adapting to different environments and hosts. During this time, they have acquired different molecules, peculiar structures, and organelles, some of which are absent in other living organisms, to successfully invade hosts, proliferate, and evade immune attacks successfully.

The existence of different stages of the same organism, which have different locations, antigenic structures, biochemical behavior, and even different morphology, makes parasites one of the most fascinating biological models. On the other hand, the use of new cellular and molecular biology strategies in addition to “omics” has made it possible to open new possibilities for understanding in detail how they interact with the host and cause disease.

This Special Issue of Pathogens will highlight recent advances in the virulence, molecular, and cell biology of human parasites with a focus on the pathogenesis of parasitic disease, molecular and cell biology, immune response and immune evasion, vaccination, and current developments and the contribution of omics, all of which provide the basis for a complete overview of modern parasitology that will enable the design of strategies for the prevention, control, and eventual eradication of parasitic infections.

Prof. Dr. Jorge Gonzalez
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • parasites
  • virulence
  • molecular cell biology
  • immunity
  • vaccination

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Published Papers (3 papers)

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Research

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13 pages, 1484 KB  
Article
Stage-Specific Expression and Subcellular Localization of Calcineurin in Infective Forms of Leishmania amazonensis
by Deborah Brandt-Almeida, Ismael Pretto Sauter, Mario Costa Cruz, Cristian Cortez, Patricio Reyes Orrego and Mauro Cortez
Pathogens 2025, 14(11), 1139; https://doi.org/10.3390/pathogens14111139 - 10 Nov 2025
Viewed by 366
Abstract
Calcineurin (CaN), a Ca2+-dependent phosphatase, plays key roles in eukaryotic cell signaling. We investigated whether Leishmania amazonensis’ two infective forms—promastigotes and amastigotes—exhibit differences in CaN expression, localization, and functional impact, using two canonical inhibitors (cyclosporin A, CsA; tracolimus, FK506). At [...] Read more.
Calcineurin (CaN), a Ca2+-dependent phosphatase, plays key roles in eukaryotic cell signaling. We investigated whether Leishmania amazonensis’ two infective forms—promastigotes and amastigotes—exhibit differences in CaN expression, localization, and functional impact, using two canonical inhibitors (cyclosporin A, CsA; tracolimus, FK506). At high 40 µM CsA, promastigotes showed reduced viability, whereas amastigotes remained resistant. FK506 had no effect on either form. At a sub-lethal 25 µM CsA, parasite proliferation remained unaffected. In parasite–macrophage co-incubation assays, phosphorylation patterns differed: amastigotes—but not promastigotes—showed increased serine/threonine phosphorylation upon CaN inhibition. Western blotting and in silico data revealed higher CaN catalytic (CaNA2) and regulatory (CaNB) subunit expression in amastigotes than promastigotes. Immunofluorescence localized CaNA prominently in both cytoplasm and nucleus of promastigotes, but predominantly cytoplasmic in amastigotes; CaNB was largely cytoplasmic in both. In silico localization predictions suggested strong membrane associations for CaNA in Leishmania, contrasting with mammalian models. Subcellular fractionation confirmed CaNA enrichment in membrane fractions, with CaNB in cytoplasmic and nuclear fractions. Collectively, these findings reveal form-specific differences in expression, subcellular distribution, and inhibitor responses of CaN in L. amazonensis, highlighting its potential as a stage-specific therapeutic target in leishmaniasis. Full article
(This article belongs to the Special Issue Virulence and Molecular Cell Biology of Parasites)
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13 pages, 1307 KB  
Article
3-Bromopyruvate Impairs Mitochondrial Function in Trypanosoma cruzi
by Rafaella Oliveira da Costa, Davi Barreto-Campos, Juliana Barbosa-de-Barros, Giovanna Frechiani, Luiz Fernando Carvalho-Kelly, Ayra Diandra Carvalho-de-Araújo, José Roberto Meyer-Fernandes and Claudia Fernanda Dick
Pathogens 2025, 14(7), 631; https://doi.org/10.3390/pathogens14070631 - 25 Jun 2025
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Abstract
Trypanosoma cruzi is a kinetoplastid parasite and etiological agent of Chagas disease. Given the significant morbidity and mortality rates of this parasitic disease, possible treatment alternatives need to be studied. 3-Bromopyruvate (3-BrPA) is a synthetic analog of pyruvate that was introduced in the [...] Read more.
Trypanosoma cruzi is a kinetoplastid parasite and etiological agent of Chagas disease. Given the significant morbidity and mortality rates of this parasitic disease, possible treatment alternatives need to be studied. 3-Bromopyruvate (3-BrPA) is a synthetic analog of pyruvate that was introduced in the early 21st century as an anticancer agent, affecting the proliferation and motility of certain microorganisms. Therefore, this work aims to evaluate the role of 3-BrPA in the energy metabolism, proliferation, and infectivity of T. cruzi, with a primary focus on the mitochondrial state, ATP production, and the key glycolytic pathway enzymes. It was observed that mitochondrial function in 3-BrPA cells was impaired compared to control cells. Accordingly, cells maintained in control conditions have a higher intracellular ATP content than cells maintained with 3-BrPA and higher ecto-phosphatase activity. However, the 3-BrPA reduced ecto-nuclease activity and was capable of hydrolyzing 5′-AMP, ADP, and ATP. When we evaluated two key glycolytic pathway enzymes, glucose kinase (GK) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), we observed that 3-BrPA induced higher GAPDH activity but did not alter GK activity. The compensatory energy mechanisms presented in T. cruzi may influence the process of cell metabolism and, consequently, the functional infectious process, suggesting the potential use of 3-BrPA in future clinical applications for Chagas disease. Full article
(This article belongs to the Special Issue Virulence and Molecular Cell Biology of Parasites)
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Review

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16 pages, 320 KB  
Review
Regulation and Roles of Metacyclogenesis and Epimastigogenesis in the Life Cycle of Trypanosoma cruzi
by Abel Sana, Izadora Volpato Rossi and Marcel Ivan Ramirez
Pathogens 2025, 14(11), 1149; https://doi.org/10.3390/pathogens14111149 - 12 Nov 2025
Viewed by 434
Abstract
Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits remarkable developmental plasticity that enables its survival across distinct environments within the insect vector and mammalian host. This review focuses on two critical differentiation processes—metacyclogenesis and epimastigogenesis—emphasising their environmental triggers, metabolic regulation, and [...] Read more.
Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits remarkable developmental plasticity that enables its survival across distinct environments within the insect vector and mammalian host. This review focuses on two critical differentiation processes—metacyclogenesis and epimastigogenesis—emphasising their environmental triggers, metabolic regulation, and roles in parasite transmission and life cycle progression. Metacyclogenesis, occurring in the hindgut of triatomine vectors, transforms replicative epimastigotes into infective metacyclic trypomastigotes and is tightly controlled by factors such as nutrient starvation, pH, and temperature. In contrast, epimastigogenesis allows trypomastigotes to revert to epimastigote forms, primarily in the vector midgut, as part of the parasite’s adaptation to vector colonisation. We compare these processes through the lens of stress-induced signalling and proteomic reprogramming, highlighting their metabolic divergence and ecological significance. Emerging evidence also suggests that extracellular vesicles (EVs) released by different parasite forms may actively modulate these transitions, supporting parasite communication and immune evasion strategies. A better understanding of these transitions provides novel insight into parasite adaptation and reveals potential molecular targets for disrupting the life cycle of T. cruzi. Full article
(This article belongs to the Special Issue Virulence and Molecular Cell Biology of Parasites)
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