From a minimal and simplified viewpoint, life is a succession of events leading to transmission of genes from parents to offspring. For certain organisms, like protozoan parasites, these events must include a meeting with someone else: another eukaryote to act as an invertebrate or vertebrate host and occasionally a human host. To get a successful gene transmission, parasites must have a positive outcome of the infection event (or series of events, as the infection for some parasites means a complex cycle between two or more hosts). But infection does not represent a one way event: it is a disruptive phenomenon, by which the metabolic balance of one organism is perturbed in favour of the survival and gene dissemination of another one, the intruder. It is thus a two sided event that implies several biochemical and immunological defense mechanisms being mounted by the host, and molecular barriers which need to be past by the parasite. If left without human intervention, this interaction would naturally proceed to a balance with no winner or loser. However, events may take a different course due to the action of external agents like medicinal drugs and vaccines, which can force the disrupted balance to return to its original configuration. From a parasite perspective, this is a kind of unnatural obstacle that they must surmount to continue their endless purpose of gene spreading.
Nothing is more reductionist than this point of view, but it is also a tempting starting point for the reasoning of why certain structures and phenomena arise in life. Think about the eukaryotes at the base of tree of life (tol.org). They still bear some of the features of what might had been the ancestoral eukaryotic cell but nonetheless have attained an impressively high level of complexity for single celled organisms. Among these “primitive” eukaryotes are some protozoa species such as Trichomonas vaginalis and Trypanosoma cruzi, which are also human parasites. Biochemical details of the molecular events in these parasites have been investigated at a slower pace than those in model eukaryotes. Besides, the peculiarities of a parasite life style implies that the general rules emerging from studies in model organisms cannot be seamlessly translated to their biological machinery. A knowledge gap becomes visible!
Two papers in the 2015 [110(7)] issue of Memórias do Instituto Oswaldo Cruz report the results of research work that contributes to filling the knowledge gap by new experimental evidence: (i) Modulatory effect of iron chelators on adenosine deaminase activity and gene expression in Trichomonas vaginalis by Primon-Barros et al. and (ii) Identification of the nicotinamide mononucleotide adenylyltransferase of Trypanosoma cruzi by Niño et al.
Currently, due to the huge amount of biological data available, understanding the mainstream knowledge for the parasite world is a kind of scientific effort that might require some level of “thought experiment” before generating experimental data in the laboratory. But be careful: noise also carries information (though random and unexpected), and smoothing data may hide the desired pattern instead!
Adeilton Alves Brandão | Editor