Abstract
Simple, reliable tools for diagnosis of human African Trypanosomiases could ease field surveillance and enhance patient care. In particular, current methods to distinguish patients with (stage II) and without (stage I) brain involvement require samples of cerebrospinal fluid. We describe here an exploratory study to find out whether miRNAs from peripheral blood leukocytes might be useful in diagnosis of human trypanosomiasis, or for determining the stage of the disease. Using microarrays, we measured miRNAs in samples from Trypanosoma brucei gambiense-infected patients (9 stage I, 10 stage II), 8 seronegative parasite-negative controls and 12 seropositive, but parasite-negative subjects. 8 miRNAs (out of 1205 tested) showed significantly lower expression in patients than in seronegative, parasite-negative controls, and 1 showed increased expression. There were no clear differences in miRNAs between patients in different disease stages. The miRNA profiles could not distinguish seropositive, but parasitologically negative samples from controls and results within this group did not correlate with those from the trypanolysis test. Some of the regulated miRNAs, or their predicted mRNA targets, were previously reported changed during other infectious diseases or cancer. We conclude that the changes in miRNA profiles of peripheral blood lymphocytes in human African trypanosomiasis are related to immune activation or inflammation, are probably disease-non-specific, and cannot be used to determine the disease stage. The approach has little promise for diagnostics but might yield information about disease pathology.
Highlights
African Trypanosomiases (AT) cause devastating diseases of livestock and humans in areas of Africa that harbor the vector, the Tsetse fly
We have identified nine miRNAs whose levels were altered in the peripheral blood of Human African trypanosomiasis (HAT) patients
We compared the patient miRNA profiles with those of subjects who were Card Agglutination Test for Trypanosomiasis (CATT)-positive, but PCR-negative, we discovered that some of the latter, too, had ‘‘HAT-like’’ miRNA profiles
Summary
African Trypanosomiases (AT) cause devastating diseases of livestock and humans in areas of Africa that harbor the vector, the Tsetse fly. Between 2000 and 2009, about 175,000 human cases were reported, the vast majority of which were caused by Trypanosoma brucei gambiense in West Africa [1]. Human African trypanosomiasis (HAT) new infection rates are currently relatively low, at about 10,000 cases per year [2] but maintenance of this level relies on continuous surveillance efforts [2]. The conventional profile of human African trypanosomiasis (HAT) includes an initial hemolymphatic stage (stage I), with no specific signs [3]. This progresses to a late stage (stage II) involving the central nervous system. Most patients eventually succumb to infection if untreated, a few cases have been reported in which patients become asymptomatic or even self-cure [4,5]
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