Commingling and Segregation analyses of seropositivity for Trypanosoma cruzi infection in Chaco Province, Argentina

NICOLÁS TOMASINI; ANAHÍ M. ALBERTI DAMATO; JUAN JOSÉ LAUTHIER; MARÍA M. MONJE RUMI; PAULA G. RAGONE; CECILIA PÉREZ BRANDAN; MIGUEL A. BASOMBRÍO; CHRISTIAN BARNABÉ; MICHEL TIBAYRENC; PATRICIO DIOSQUE

Ascochinga

Congreso; XXIV Reunión Científica Anual de la Sociedad Argentina de Protozoología; 2010

Sociedad Argentina de Protozoologia

The wide range of clinical outcomes in Chagas Disease and the different risks of infection by Trypanosoma cruzi in different families can be attributed not only to the genetic polymorphism among different parasite stocks and the shared environmental factors but also to human genetic variability. Little is known about the existence of a major gene influencing the susceptibility to infection in humans by this parasite. The goal of this study was to investigate the inheritance model that best fits the observed distribution pattern of seropositivity to T. cruzi among 205 members of 21extended pedigrees in a rural area of Chaco province in Argentina. Using S.A.G.E software package we carried out a comminling analysis and a complex segregation analysis of seropositivity by fitting different genetic hypothesis-based regressive multivariate logistic models adjusting or not with different co-variables. We evaluated the likelihood of sporadic, different major gene, environmental and general models. Comparisons between models were carried out using the likelihood ratio test and Akaike information criterion. We observed in the commingling analysis the data was better explained by two-distributions when age of individuals, presence of intradomiciliary triatomine bugs and construction types were considered as covariates. This analysis weakly suggests the existence of a major gene influencing the phenotype. In the segregation analysis we observed that models with estimation of familiar association parameters have better fitting than models without considering them, supporting familiar aggregation of the phenotype. Additionally, the general model does not fit significantly better than some mendelian models. All these results are in accord with a genetic component in the susceptibility to the infection and support the major gene hypothesis. We are actually expanding the number of pedigrees to analyze in order to obtain a better sample size.