In this study we investigated the possible role of two CCR5 gene polymorphi
sms, CCR5 Delta 32 deletion and CCR5 59029 A -->G promoter point mutation,
in determining the susceptibility to Trypanosoma cn,(Zi infection as well a
s in the development of chagasic heart disease. These CCR5 polymorphisms we
re assessed in 85 seropositive (asymptomatic, n=53; cardi- omyopathic, n=32
) and 87 seronegative individuals. The extremely low frequency (0.009) of t
he CCR5 Delta 32 allele in our population did not allow us to analyse its p
ossible influence on T cruzi infection. We found no differences in the dist
ribution of CCR5 59029 promoter genotype or phenotype frequencies between t
otal chagasic patients and controls. However, we observed that the CCR5 590
29-A/G genotype was significantly increased in asymptomatic with respect to
cardiomyopathic patients (P=0 02; OR=0 33 95% CI 0.10- 0.94). In addition,
the presence of the CCR5 59029-G allele was also increased in asymptomatic
s when compared with cardiomyopathics (P=0 02;. OR=0.35, 95% CI 0.12-0.96).
Our data suggest that the CCR5 59029 promoter polymorphism may be involved
in a differential susceptibility to chagasic cardiomyopathy.