Cellular Interactions between Protozoan Pathogens and Hosts

A special issue of Tropical Medicine and Infectious Disease (ISSN 2414-6366). This special issue belongs to the section "Vector-Borne Diseases".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 11789

Special Issue Editor


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Guest Editor
Department of Tropical Medicine, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA
Interests: protozoan parasites; medical protozoology; cell and molecular biology of malaria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Protozoan pathogens are responsible for several important human and animal diseases. Included among these diseases are malaria, African trypanosomiasis, Chagas disease, leishmaniasis, amebiasis, giardiasis, trichomoniasis, toxoplasmosis, cryptosporidiosis, and other coccidioses. Even though protozoa are single-cell eukaryotic organisms, these various pathogenic protozoa are quite distinct from each other in regards to their genetics and cell biology, and many exhibit unique cellular features not found in their hosts. Some of these unique features are highly specialized mechanisms by which they interact with their hosts, and in some cases vectors. These specialized adaptations facilitate infection of the host, survival within the host, and transmission to other hosts. Quite often these interactions involve cell-cell accociations between the protozoan and host via unique structures or proteins, which may also contribute to disease pathogenesis. A better understanding of these host-pathogen interactions at a cellular and molecular levels may facilitate the development of novel therapeutic approaches in treating and controlling these diseases.

This special issue will explore cellular interactions between protozoan pathogens and their hosts. This can include characterization of interactions at the ultrastructural or molecular levels, as well as the genes involved in these interactions. Interactions can include adherence between host and pathogen, modification of the host by the pathogen, or damage to the host caused by the pathogen.

You may choose our Joint Special Issue in Life.

Dr. Mark F. Wiser
Guest Editor

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Keywords

  • Protozoa
  • Protozoal disease
  • Host-parasite interaction
  • Adherence
  • Invasion
  • Secretion
  • Receptor-ligand interactions
  • Pathogenesis

Published Papers (2 papers)

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Research

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26 pages, 7897 KiB  
Article
Colpodella sp. (ATCC 50594) Life Cycle: Myzocytosis and Possible Links to the Origin of Intracellular Parasitism
by Troy A. Getty, John W. Peterson, Hisashi Fujioka, Aidan M. Walsh and Tobili Y. Sam-Yellowe
Trop. Med. Infect. Dis. 2021, 6(3), 127; https://doi.org/10.3390/tropicalmed6030127 - 11 Jul 2021
Cited by 5 | Viewed by 5114
Abstract
Colpodella species are free living bi-flagellated protists that prey on algae and bodonids in a process known as myzocytosis. Colpodella species are phylogenetically related to Apicomplexa. We investigated the life cycle of Colpodella sp. (ATCC 50594) to understand the timing, duration and the [...] Read more.
Colpodella species are free living bi-flagellated protists that prey on algae and bodonids in a process known as myzocytosis. Colpodella species are phylogenetically related to Apicomplexa. We investigated the life cycle of Colpodella sp. (ATCC 50594) to understand the timing, duration and the transition stages of Colpodella sp. (ATCC 50594). Sam-Yellowe’s trichrome stains for light microscopy, confocal and differential interference contrast (DIC) microscopy was performed to identify cell morphology and determine cross reactivity of Plasmodium species and Toxoplasma gondii specific antibodies against Colpodella sp. (ATCC 50594) proteins. The ultrastructure of Colpodella sp. (ATCC 50594) was investigated by transmission electron microscopy (TEM). The duration of Colpodella sp. (ATCC 50594) life cycle is thirty-six hours. Colpodella sp. (ATCC 50594) were most active between 20–28 h. Myzocytosis is initiated by attachment of the Colpodella sp. (ATCC 50594) pseudo-conoid to the cell surface of Parabodo caudatus, followed by an expansion of microtubules at the attachment site and aspiration of the prey’s cytoplasmic contents. A pre-cyst formed at the conclusion of feeding differentiates into a transient or resting cyst. Both DIC and TEM microscopy identified asynchronous and asymmetric mitosis in Colpodella sp. (ATCC 50594) cysts. Knowledge of the life cycle and stages of Colpodella sp. (ATCC 50594) will provide insights into the development of intracellular parasitism among the apicomplexa. Full article
(This article belongs to the Special Issue Cellular Interactions between Protozoan Pathogens and Hosts)
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Review

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12 pages, 914 KiB  
Review
Apicortin, a Constituent of Apicomplexan Conoid/Apical Complex and Its Tentative Role in Pathogen—Host Interaction
by Ferenc Orosz
Trop. Med. Infect. Dis. 2021, 6(3), 118; https://doi.org/10.3390/tropicalmed6030118 - 30 Jun 2021
Cited by 5 | Viewed by 4945
Abstract
In 2009, apicortin was identified in silico as a characteristic protein of apicomplexans that also occurs in the placozoa, Trichoplax adhaerens. Since then, it has been found that apicortin also occurs in free-living cousins of apicomplexans (chromerids) and in flagellated fungi. It [...] Read more.
In 2009, apicortin was identified in silico as a characteristic protein of apicomplexans that also occurs in the placozoa, Trichoplax adhaerens. Since then, it has been found that apicortin also occurs in free-living cousins of apicomplexans (chromerids) and in flagellated fungi. It contains a partial p25-α domain and a doublecortin (DCX) domain, both of which have tubulin/microtubule binding properties. Apicortin has been studied experimentally in two very important apicomplexan pathogens, Toxoplasma gondii and Plasmodium falciparum. It is localized in the apical complex in both parasites. In T. gondii, apicortin plays a key role in shaping the structure of a special tubulin polymer, conoid. In both parasites, its absence or downregulation has been shown to impair pathogen–host interactions. Based on these facts, it has been suggested as a therapeutic target for treatment of malaria and toxoplasmosis. Full article
(This article belongs to the Special Issue Cellular Interactions between Protozoan Pathogens and Hosts)
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