Cellular and Molecular Basis of Parasite Infection

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 605

Special Issue Editors


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Guest Editor
D’Youville University, Buffalo, NY 14201, USA
Interests: parasitic diseases; communicable diseases; infectious disease prevention and control

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Guest Editor
School of Public Health and Health Sciences, College of Health, Human Services and Nursing, California State University Dominguez Hills, Carson, CA, USA
Interests: parasitic diseases; public health; communicable diseases
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Special Issue Information

Dear Colleagues,

Parasite infections are complex biological processes that involve intricate interactions between the parasite and the host at both cellular and molecular levels. Understanding these interactions is crucial for developing effective treatments and preventive measures. At the cellular level, parasites often invade host cells, utilizing the host's cellular machinery to replicate and evade the immune system. For instance, Plasmodium, the parasite responsible for malaria, invades red blood cells and modifies their surface proteins to avoid detection.

On a molecular level, parasites secrete various molecules that manipulate host cell functions. These molecules can interfere with signaling pathways, immune responses, and cellular metabolism. For example, the Trypanosoma brucei parasite, which causes African sleeping sickness, uses a process called antigenic variation to change its surface glycoproteins, helping it evade the host's immune system.

Research in this field focuses on identifying the specific cellular and molecular mechanisms parasites use to infect hosts and how hosts respond to these infections. This knowledge is essential for developing new drugs, vaccines, and diagnostic tools to combat parasitic diseases.

Dr. Adekunle Sanyaolu
Dr. Ricardo Izurieta
Guest Editors

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Keywords

  • parasite infection
  • host–parasite interaction
  • cellular invasion
  • molecular mechanisms
  • immune evasion

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Published Papers (1 paper)

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Research

13 pages, 1376 KB  
Article
The Role of BRCT Domain from LmjPES in Leishmania major Pathogenesis
by Esther Larrea, José Peña-Guerrero, Celia Fernández-Rubio, Aroia Burguete-Mikeo, Elizabeth Guruceaga and Paul Nguewa
Biomolecules 2025, 15(8), 1191; https://doi.org/10.3390/biom15081191 - 19 Aug 2025
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Abstract
Leishmaniasis is caused by protozoan parasites from the genus Leishmania and remains one of the major threats to global health, impacting millions of people worldwide as well as animals including dogs. Several treatments have been used for managing leishmaniasis; nevertheless, drug resistance has [...] Read more.
Leishmaniasis is caused by protozoan parasites from the genus Leishmania and remains one of the major threats to global health, impacting millions of people worldwide as well as animals including dogs. Several treatments have been used for managing leishmaniasis; nevertheless, drug resistance has emerged as an important obstacle to disease control. Therefore, there is an urgent need to discover new therapeutic targets. The aim of this work was to study the role played by the breast cancer associated 1 C-terminal (BRCT) domain from LmjPES protein (Pescadillo ribosomal biogenesis factor) in Leishmania major‘s pathogenesis through the construction of novel genomic tools. For this purpose, Leishmania integrative plasmids that were able to express the BRCT domain from LmjPES and a hypothetical defective LmjPES lacking this BRCT domain were constructed. It was observed that the overexpression of the aforementioned BRCT domain in L. major dysregulated the mRNA expression of 152 genes (95 up-regulated and 57 down-regulated) in respect to control parasites. Furthermore, clustering studies of these altered genes revealed an enrichment in genes related to metabolic processes, transporter activity, response to stimuli, and protein folding, which are categories described to be associated with the metacyclogenesis process and parasite survival. Interestingly, these genes reached normal levels of expression in parasites transfected with a defective LmjPES (a mutated gene lacking the coding sequence of the BRCT domain). In addition, it was found that the footpad of mice inoculated with LmjPES BRCT-overexpressing parasites had significantly greater inflammation compared to the size of the footpad of animals infected with the control parasites. Based on all these results, it was suggested that the BRCT domain from LmjPES might play a role in L. major‘s infection process and pathogenesis. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Parasite Infection)
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