The languages of parasite communication

Abstract

Although it is regarded as self-evident that parasites interact with their hosts, with the primary aim of enhancing their own survival and transmission, the extent to which unicellular parasites communicate with each has been severely underestimated.Recent publications show that information is commonly exchanged between parasites of the same species and that this can govern their decisions to divide, to differentiate or to migrate as a group. Communication can take the form of soluble secreted factors, extracellular vesicles or contact between cells. Extracellular parasites can do this directly, while intracellular parasites use the infected host cell -or components derived from it -as an intermediary. By emitting signals that can be dispersed within the host, parasites can also have long-distance effects on the course of an infection and its pathology. This article presents an overview of recent developments in this field and draws attention to some older work that merits re-examination. 3 Most readers of this article will not need to be told that diseases such as sleeping sickness, malaria, Leishmaniasis, Trichomoniasis and Chagas Disease are caused by unicellular parasites. This knowledge might come with the tacit assumption that singlecelled organisms are completely self-sufficient and have no need to interact, much less cooperate, with members of their own species. In recent years, however, it has become apparent that a number of decisions are group decisions that rely on parasites communicating with each other. Just as animals can exchange information in different ways, be it vocally, visually, chemically or by body language, parasites have also developed a range of mechanisms for communicating with each other. This sometimes occurs directly, from parasite to parasite, or by using the infected host cell -or components derived from it -as an intermediary. By emitting signals that can be dispersed within the host, parasites can also have wide-ranging effects on the course of an infection and its pathology. This article presents an overview of recent developments in this field and draws attention to some older work that merits re-examination. Owing to space constraints, it will not cover molecules used by intracellular parasites to reprogram the cells that they infect. Quorum sensing and differentiationDifferent subspecies of Trypanosoma brucei, the pathogens responsible for human sleeping sickness and Nagana in domestic animals, are extracellular throughout their life cycle. In the mammalian host the parasites use a quorum sensing mechanism to maintain a balance between slender bloodstream forms, which are capable of dividing every 6-8 hours, and stumpy bloodstream forms, which cannot divide and have a lifespan of a few days. When trypanosomes ingested by a tsetse fly, the slender form is killed while the stumpy form survives and differentiates to the next life stage, the procyclic form, in the insect midgut [1,2]. If slender forms were to proliferate unchecked, this would result in rapid death of th...

Perils and Promises of Pathogenic Protozoan Extracellular Vesicles

“…Unassumingly, T. cruzi-derived vesicles may influence parasite proteolytic activity on the host tissue (Torrecilhas et al, 2009). However, the lytic effect of purified T. cruzi vesicles on host cells was transiently local to the site of inoculation in mice, suggesting that not all the RBCs in the circulation are equally vulnerable or probably lack certain corresponding molecular signatures (Roditi, 2016).…”

“…The formation and release of vesicles enhance survival, transmission, and mitotic multiplication of pathogenic protozoa (Roditi, 2016 ). Also, vesicle-dependent and proportional 5-fold increase in absolute number of T. cruzi trypomastigote suggests that parasite-derived vesicles could initiate parasite replication (Garcia-Silva et al, 2014 ).…”

“…T. cruzi -derived vesicles have been suggested to be endocytosed by host cells (Bayer-Santos et al, 2013 ). Hypothetically, vesicular content can be delivered to host cells through fusion of EVs with the host cell, endocytotic assimilation, or progressively by a control-delivery system (Roditi, 2016 ; Li et al, 2018b ). The sequence of PPEV internalization might involve binding to host cells through receptor–ligand interactions, and in the process become putatively attached to the target-cell membranes before endocytosis (Valadi et al, 2007 ).…”

Discrimination Experiments in Entamoeba and Evidence from Other Protists Suggest Pathogenic Amebas Cooperate with Kin to Colonize Hosts and Deter Rivals

“…), habitat/niche partitioning within the host by colonizing distinctive host environments (Ramiro et al. ), or cooperative behaviors with kin, like social motility in Trypanosoma (SoMo, below), which exclude unrelated cells (Roditi ; Roditi et al. ).…”

Non-coding RNAs in Host–Pathogen Interactions: Subversion of Mammalian Cell Functions by Protozoan Parasites

“…Protozoan parasite-host cell interplay can occur directly by physical cell-cell contact or indirectly via secreted/excreted molecules, which can be released into the extracellular medium or packed into extracellular vesicles (EVs) (reviewed in Torrecilhas et al, 2012; Barteneva et al, 2013; Deolindo et al, 2013; Mantel and Marti, 2014; Marcilla et al, 2014; Judice et al, 2016; Marti and Johnson, 2016; Roditi, 2016; Szempruch et al, 2016a; Watanabe Costa et al, 2016). The packaging of proteins and nucleic acids, such as small non-coding RNAs (sncRNAs), in EVs protects them from extracellular degradation until they reach the target recipient cell.…”