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African and American trypanosomes are unable to synthesize sialic acids (SA). They acquire thesugar from hosts glycoconjugates by transferring it to their acceptor molecules by the trans-sialidases (TS), enzymes known to be virulence factors. At variance with Trypanosoma cruziwhich express one TS (TScruzi), T. congolense express four TS (TScon) in the trypomastigotestage. We conducted a comparative analysis of some of these enzymes, using recombinantTScon 1-3 and TScruzi. We evaluated: 1- their enzymatic activity: testing two sialyl donors,3?SL [Neu5Ac-α(2,3)-lactose] and azidosialyl-α(2,3)galactose-ßO-Met, and as acceptor [ 14 C]-lactose. We found that TScruzi as well as TScon1a, TScon1b y TScon2 were able to transfer SAfrom 3?SL donor to the acceptor displaying similar enzymatic properties, while TScon3 wasinactive with this substrate. However, TScon3 transferred the SA azido modified (fromazidosialyl-α(2,3)galactose-ßO-Met) similarly as TScruzi does, while TScon1 and 2 wereinactive. 2- their stability in mice bloodstream: TScon1a and TScon2 enzymes wereintravenously (iv) administered (5 μg) and their activity were analysed in blood samples at 0,5-and 15-min post-administration (pa). TScon1a and TScon2 activities drop and remaindetectable only for 15 min. TScruzi remained in circulation during days. The presence ofcirculating forms as the only stage in mammals, high parasitemia levels and continuous TSshedding suggest that developing strategies to support the enzymes for long in blood isunnecessary. 3- Effect on mouse platelets: Five μg of TScon1b and TScon2 were administerediv in two doses. Platelets were counted at 18h pa and again after 18h of a second dose.TScon1b induced significant thrombocytopenia after both doses, TScon2 only after the seconddose. We have shown that by desialylation of platelet surface molecules, TScruzi inducethrombocytopenia. In assays 2 and 3, PBS-BSA 1% was used as control.