Despite the wealth of information generated by trans-disciplinary
research in
Chagas disease,
knowledge about its multifaceted
pathogenesis is still fragmented. Here we
review the body of
experimental studies in
animal models supporting the concept that
persistent infection by
Trypanosoma cruzi is crucial for the development of chronic
myocarditis. Complementing this
review, we
will make an effort to reconcile seemingly contradictory results concerning the immune profiles of chronic
patients from
Argentina and
Brazil. Finally, we
will review the results of molecular studies suggesting that
parasite-induced
inflammation and
tissue damage is, at least in part, mediated by the activities of trans-
sialidase,
mucin-linked
lipid anchors (TLR2
ligand) and cruzipain (a
kinin-releasing
cysteine protease). One hundred years after the discovery of
Chagas disease, it is reassuring that basic and clinical
research tends to converge, raising new perspectives for the
treatment of chronic
Chagas disease.