Abstract
Host genetic factors exert significant influences on differential susceptibility to many infectious diseases. In addition, population structure of both host and parasite may influence disease distribution patterns. In this study, we assess the effects of population structure on infectious disease in two populations in which host genetic factors influencing susceptibility to parasitic disease have been extensively studied. The first population is the Jirel population of eastern Nepal that has been the subject of research on the determinants of differential susceptibility to soil-transmitted helminth infections. The second group is a Brazilian population residing in an area endemic for Trypanosoma cruzi infection that has been assessed for genetic influences on differential disease progression in Chagas disease. For measures of Ascaris worm burden, within-population host genetic effects are generally more important than host population structure factors in determining patterns of infectious disease. No significant influences of population structure on measures associated with progression of cardiac disease in individuals who were seropositive for T. cruzi infection were found.
Highlights
The rural Posse region of Goias, Brazil is endemic for Chagas disease with approximately 50 per cent of the adult population being seropositive for T. cruzi infection [9]
The results of the analyses presented here demonstrate the value of considering population structure effects on variation in parasitic disease burden
Evidence for population structure effects may be informative for understanding the importance of genetic variation in the parasite itself
Summary
(c) Effect of Jirel population structure on Ascaris worm burden While our models included host withinpopulation genetic variation, there is the possibility that some genetic between-group variation influences worm burden measures. Because of the relative lack of evidence for embedded genetic structure in the Jirel population (as observed by the small eigenvalues obtained during the PC analysis), we limited formal testing of population structure to the first two PCs. As with our previous analyses, we included covariates such as sex, age, number of days sampled post-albendazole treatment and sex ratio of worms (for Ascaris weight only).
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