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Pathogenic mechanisms of Chagas' disease reactivation in AIDS patients

The diversity of clinical manifestations of Chagas’ disease in humans has been attributed to the host’s immune response and to the genetic heterogeneity of the parasite which may be formed by a multiclonal population with various biological profiles.10,22 The preferential location of T. cruzi in the central nervous system (CNS) may be associated with the presence of subpopulations with neurotropic characteristics that may be reactivated during the immunosuppresion of the host. Patients with HIV infection, does not lead to new T. cruzi genotypes, because T. cruzi stocks isolated from these patients were closely related to clonal genotypes previously identified (genotypes 30 or 32) in 89% and 94% of the stocks isolated from HIV-positive and HIV-negative patients, respectively.23 Reactivation of Chagas’ disease does not occur spontaneously and is strongly associated with immunosuppresion in patients who have onchohematologic neoplasms,24 those chronically treated with high doses of corticosteroids, and those with advance HIV-AIDS disease.25 In these groups of immunocompromised patients chronically infected by T. cruzi, it is possible that the parasite load can increase and the detection of parasitemia is more frequent.26,27

In this context, and especially in AIDS patients, the high level of parasitemia is related to the development of acute CNS or heart disease. However, the relation between T. cruzi parasitemia and organ damage is not absolute; sometimes we can see that severe disease is associated without detectable parasitemia. In these patients it is necessary to obtain biopsy smears to achieve a definitive diagnosis. , ,

T. cruzi displays a relevant genetic variability demonstrated by at least six discrete typing units (DTUs) from TcI to TcVI. Evidence of the impact of this genetic variability on HIV coinfection is scarce. However, some studies have suggested a differential tissue tropism of the infecting DTUs; these studies have reported mixed infections in coinfected patients, observing TcI and TcII, or TcI, TcV, and TcVI in blood, and only monoclonal TcI in cerebrospinal fluid (CSF) or brain tissue.29

 
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