Genetic predisposition to high infections in an endemic area of Schistosoma mansoni

Abel, Laurent; Dessein, Alain

doi:10.1590/s0037-86821991000100001

Cited by 11 publications

(4 citation statements)

References 6 publications

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“…Previous studies have established a precedent for the role of major genes on the variation in infection intensity. [32][33][34][35][36] However, unlike previous genetic studies, the current analysis does not assume any specific distribution of gene effects. Instead, we assesses the aggregate effect of host additive genetic factors on the variation in fecal egg counts by using a novel variance component approach 29 to partition the total variance in fecal egg counts during S. mansoni infection among explicitly quantifiable effects due to (i) host additive genetics (polygenic model), (ii) shared residence (household model), and (iii) host-specific environmental factors.…”

Section: Discussionmentioning

confidence: 99%

Additive host genetic factors influence fecal egg excretion rates during Schistosoma mansoni infection in a rural area in Brazil.

Bethony¹,

Williams²,

Blangero³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. This study quantifies the influence of shared household and kinship on egg counts during Schistosoma mansoni infection in a sample from rural Brazil. Detailed genealogic information allowed assignment of 597 individuals to 6 multihousehold pedigrees residing in 145 households. A variance component method was used to partition egg counts into shared household, additive genetic, and individual-specific environmental effects. Host additive genetic effects consistently accounted for a large proportion of the variation in egg counts: 43% in an unadjusted model and 40% in model adjusted for covariates. In a model that examined the confounding of shared household with kinship, additive genetic effects still accounted for 27% of the variation in egg counts and shared household only 12%. The consistently important role for host additive genetic factors on the variation in egg counts points to new ways of modeling and understanding the mechanisms that contribute to trait variation during infection with S. mansoni.

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Section: Discussionmentioning

confidence: 99%

Additive host genetic factors influence fecal egg excretion rates during Schistosoma mansoni infection in a rural area in Brazil.

Bethony¹,

Williams²,

Blangero³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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“…Moreover in endemic areas of schistosomiasis, it was observed that individuals with the highest infection levels were grouped within certain families, rather than randomly distributed and that certain subjects were clearly predisposed to reinfections [ 15 ]. This suggested that human resistance to infection by Schistosoma may also depend on the effects of some genetic factors [ 15 , 22 - 24 ].…”

Section: Multiple Factors Are Involved In Human Resistance To Schistomentioning

confidence: 99%

Recent Advances in the Characterization of Genetic Factors Involved in Human Susceptibility to Infection by Schistosomiasis

Isnard¹,

Chevillard

2008

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Human resistance to infection by schistosomes is associated to a strong Th2 immune. However a persistent Th2 response can cause severe kidney and liver disease in human. In this review, we mainly focused on the control of infection levels caused by schistosomes. Several experimental models allowed us to better understand the immunological mechanisms of the host against schistosome infection. High IgE and eosinophil levels are associated with resistance to infection by schistosomes and this effect is counterbalanced by IgG4. IgE and eosinophils are highly dependent on IL-4, IL-13, and Il-5, which are three main Th2 cytokines. We also examined the genetic factors involved in human susceptibility to infection by schistosomiasis. Infection levels are mainly regulated by a major locus SM1, in 5q31-q33 region, which contains the genes encoding for the IL-4, IL-13, and Il-5 cytokines. An association between an IL13 polymorphism, rs1800925, and infection levels has been shown. This polymorphism synergistically acts with another polymorphism (rs324013) in the STAT6 gene, encoding for the signal transducer of the IL13 pathway. This pathway has also been involved in atopic disorders. As helminthiasis, atopy is the result of aberrant Th2 cytokine response to allergens, with an increased production of IL-4, IL-13, Il-9 and Il-5, with high amounts of allergen-specific and total IgE and eosinophilia. However, the Th2 immune response is protective in helminthiasis but aggravating in atopic disorders. Several studies reported interplay between helminthic infections and allergic reactions. The different results are discussed here.

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“…Genetic factors also seem to predispose certain individuals to developing hepatosplenic schistosomiasis (Abel & Dessein 1991).…”

mentioning

confidence: 99%

Hepatosplenic schistosomiasis in field-based studies: a combined clinical and sonographic definition

Lambertucci

Cota

Pinto-Silva

et al. 2001

Mem. Inst. Oswaldo Cruz

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Genetic predisposition to high infections in an endemic area of Schistosoma mansoni

Cited by 11 publications

References 6 publications

Additive host genetic factors influence fecal egg excretion rates during Schistosoma mansoni infection in a rural area in Brazil.

Additive host genetic factors influence fecal egg excretion rates during Schistosoma mansoni infection in a rural area in Brazil.

Recent Advances in the Characterization of Genetic Factors Involved in Human Susceptibility to Infection by Schistosomiasis

Hepatosplenic schistosomiasis in field-based studies: a combined clinical and sonographic definition

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