Genetic and Household Determinants of Predisposition to Human Hookworm Infection in a Brazilian Community

Abstract

Background Predisposition to heavy or light human hookworm infection is consistently reported in treatment-reinfection studies. A significant role for host genetics in determining hookworm infection intensity has also been shown, but the relationship between host genetics and predisposition has not been investigated. Methods A treatment-reinfection study was carried out on 1302 individuals in Brazil. Bivariate variance components analysis was used to estimate heritability for pretreatment and reinfection intensity, and to estimate the contribution of genetic and household correlations between phenotypes to the overall phenotypic correlation (i.e. predisposition). Results Heritability for hookworm egg count was 17% pretreatment and 25% after reinfection. Predisposition to heavy or light hookworm infection was observed, with a phenotypic correlation of 0.34 between pretreatment and reinfection intensity. This correlation was reduced to 0.23 after including household and environmental covariates. Genetic and household correlations were 0.41 and 1 respectively, and explained 88% of the adjusted phenotypic correlation. Conclusions Predisposition to human hookworm infection in this area results from a combination of host genetics and consistent differences in exposure, with the latter explained by household and environmental factors. Unmeasured individual-specific differences in exposure did not contribute to predisposition.

Estimation of genetic parameters for resistance to gastro-intestinal nematodes in pure blood Arabian horses

“…However, restricting the dataset to only the egg counts from adults (horses older than 3 years) resulted in an increased heritability of 0.21. This value is consistent with the usual range of 0.20-0.40 for faecal egg excretion found in small ruminants (Davies et al, 2006;Kemper et al, 2011;Sallé et al, 2012;Assenza et al, 2014) or other host-nematode systems such as hookworm infections in humans Quinnell et al, 2010), ascaridiosis in humans (Williams-Blangero et al, 1999, 2002 or pigs (Nejsum et al, 2009). This also corroborates the age-dependent excretion pattern of strongyle eggs in horses (Chapman et al, 2003;Relf et al, 2012;Wood et al, 2012).…”

Spatial and Genetic Epidemiology of Hookworm in a Rural Community in Uganda

“…To date, the only study to investigate heritability in an African setting, conducted in Zimbabwe, suggested heritability of hookworm infection intensity was 0.37, although this study failed to account for household effects, limiting interpretation of findings. Our analysis suggested that, after accounting for household effects and covariates, heritability in this Ugandan population is relatively modest at 0.11, comparable to findings from Papua New Guinea [12] but lower those reported by studies conducted in high transmission settings in Brazil (0.20–0.25) ( Bethony , unpublished data )[13]. Heritability is a population-specific measure, and as such direct comparison of genetic contributions between sites can be confounded by both the differing importance of environmental factors and by variation in genetic polymorphisms of the pathogen/host [46], [47].…”

Human helminth co-infection: No evidence of common genetic control of hookworm and Schistosoma mansoni infection intensity in a Brazilian community

“…Similarly, water contact was a significant risk factor for both S. japonicum, T. trichiura and A. lumbricoides in the Poyang Lake region in China (Ellis et al, 2007). Interestingly, there was very little role for individual-level factors in determining predisposition to hookworm infection in this Brazilian community, suggesting that environmental determinants of co-infection may be variable through time (Quinnell et al, in press). Alternatively, the unexplained correlation between N. americanus and S. mansoni infection intensity may reflect a direct biological or immunological interaction between species.…”