Abstract
This chapter states that the term “integrated genetic epidemiology” has been coined to designate the approach consisting in simultaneously analyzing the impact of the host's, the pathogen's, and the vector's genetic diversity on the transmission and severity of infectious diseases as well as the coevolution processes between the three. It briefly summarizes what is presently known about: (i) human genetic susceptibility to Chagas disease, (ii) the vectors' species and population diversity, and (iii) the parasite's genetics and evolution. Chagas disease is a very serious illness. After infection by the parasite, patients develop an acute phase, which actually corresponds to parasitic septicemia. The most worrisome symptom is Chagasic cardiopathy, which leads to a severe cardiac insufficiency. The causative agent of Chagas disease is a parasitic protozoan of the family Kinetoplastidae. Trypanosoma cruzi is transmitted by “true” bugs. Human genetic susceptibility to Chagas disease is less well known than for other transmissible diseases such as Hepatitis C, TB, malaria, AIDS, leprosy, schistosomiasis and visceral leishmaniosis. Chagas disease strikes populations that are ethnically very diverse. Latin Americans have European, African, Amerindian, and mixed ancestries. It has now been determined that the HLA supergene complex of several genes having a related role plays an important role in the transmission, severity, and clinical diversity of Chagas disease. Chagas disease exhibits a specific epidemiological feature, namely, that the parasite can be transmitted by an impressive range of different vectors. The interpretation of isoenzyme diversity in terms of population genetics and evolutionary biology has made it possible to clarify the evolutionary status of the zymodemes. When natural cycles are considered, possible protocols could be to compare T. cruzi genotypes isolated from (i) cardiac versus digestive versus ASY patients, (ii) different mammal species, and (iii) different triatomine bug species.
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