Abstract
One hundred and seventy-seven individuals belonging to 120 complete or incomplete nuclear families from Bambui, in the State of Minas Gerais, southeastern Brazil, were studied in order to examine causes of variation in the eosinophil rate among subjects infested by intestinal worms with an extra-digestive cycle. Segregation analysis without correction for skewness showed that the hypothesis of the presence of an additive major gene was consistent with the data, although a dominant, recessive, or a multifactorial hypothesis could not account properly for the observed significant familial aggregation. The most parsimonious correction for skewness showed similar results, but could not distinguish between dominant and recessive models, although co-dominance was rejected. Since these models assume that skewness was attributable to the commingling of two distributions, these results seem to agree with those for uncorrected data. These findings suggest that several genetically independent factors determine the resistance/susceptibility to helminth infestation mainly through their ability to influence the eosinophil response.
Highlights
The sample was divided into subjects without parasites and those with at least one of the internal parasites (Ascaris lumbricoides, Strongyloides stercoralis, Ancylostomids and/or Schistosoma mansoni)
To investigate the effects of sex and age on eosinophil rate, regression analyses were done on the entire sample and on the parasitized sub-group
Because of the skewness of the distributions and the large variance values, the stepwise multiple regressions were done using the natural logarithms of the eosinophil rate (LER) and the independent variables sex, age, age squared and sex-age interactions
Summary
Several studies have reported the existence of important genetic mechanisms acting on phenotypes involved in certain human responses possibly related to resistance/ susceptibility to malaria (Abel et al, 1992a), tegumentary (Shaw et al, 1995; Alcaïs et al, 1997) and visceral (Feitosa et al, 1998) leishmaniasis, leprosy (Abel and Demenais, 1988; Abel et al, 1989, 1992ab, 1995; Feitosa et al, 1995a,b, 1996) and schistosomiasis mansoni (Abel et al, 1991; Marquet et al, 1996; Müller-Myhsok et al, 1997). The capacity for eosinophilia probably has a major role in the resistance to parasitic infestations that trigger this response. The presence of a major gene responsible for setting up the eosinophil response to helminthic infestation has been reported for rodents In humans, Moro-Furlani and Krieger (1992) demonstrated that in three Brazilian samples the familial resemblance of eosinophil levels resulted from biological transmission rather than shared environmental factors. These conclusions were based on a series of familial correlations. We examined the causes of this biological mechanism, using commingling and segregation analyses, applied to one of the above Brazilian samples
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