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PubMed1983

Purified Trypanosoma cruzi specific glycoprotein for discriminative serological diagnosis of South American trypanosomiasis (Chagas' disease).

Chagas' disease, leishmaniasis, and Trypanosoma rangeli infection are endemic and their distributions overlap in vast regions of South and Central America. Serological cross-reactivities can confuse epidemiological studies of these infections, and their differential diagnosis has been assigned a high priority by the World Health Organisation. A lectin-affinity-purified, 90,000 molecular weight glycoprotein (GP90) is present in the known principal strains (zymodemes) of Trypanosoma cruzi and absent from Leishmania and T rangeli. Patients with T cruzi infection have antibody to GP90, whereas patients with leishmaniasis do not and the two infections can be distinguished in an ELISA system using this antigen. In a mouse model, the same test can differentiate between T cruzi and T rangeli infections. Antigens purified by affinity chromatography clearly provide a practical basis for very precise, even strain-specific, diagnostic tests.

Antibodies↗
PubMed1984

Immunological consequences of infection and vaccination in South American trypanosomiasis.

Trypanosoma cruzi infection provokes a vigorous immune response that terminates the parasitaemia associated with the acute stage within two to three months of initial infection. Even so, a variable proportion of patients may develop severe Chagas' disease, often decades after initial infection. Recent experimental findings suggest that trypomastigotes of T. cruzi possess a surface bound neuraminidase and sugar binding protein by means of which they invade host cells--a mechanism very reminiscent of influenza virus. Studies of the antibody response to trypomastigotes in patients or murine models have identified a series of antibodies able to mediate lysis of live parasites in a complement mediated lysis (c.m.l.) assay. These antibodies have also been linked to resistance to infection in vivo and disappear following successful parasitological 'cure' in drug-treated animals and human patients. Immunochemical studies have shown that sera from infected patients or mice lacking this c.m.l. activity also lack those antibodies able to bind trypomastigote surface components of 85 and 160 kDa relative molecular mass. The availability of rabbit and mouse models of Chagas' disease have produced data that suggest that chronic stage pathology may have an immunological basis dependent on the known cross reactivity between host and parasite cells. Delivery of the lethal hit leading to host cell destruction is probably facilitated by the ability of parasite antigens to bind to host cells thus exposing them to the host's own anti-parasite immune response. If Chagas' disease does indeed have an immunological basis, then this might be controlled in turn by immunoregulation, in a manner analogous to that achieved in experimental allergic encephalomyelitis.

Animals↗