Genetics of susceptibility to human helminth infection.
Recent studies have shown that host genetics is an important determinant of the intensity of infection and morbidity due to human helminths. Epidemiological studies of a number of parasite species have shown that the intensity of infection (worm burden) is a heritable phenotype. The proportion of variance in human worm burden explained by genetic effects varies from 0.21 to 0.44. Human genome scans have identified a locus responsible for controlling Schistosoma mansoni infection intensity on chromosome 5q31-q33, and loci controlling Ascaris lumbricoides intensity on chromosomes 1 and 13, although the genes involved have not yet been identified. There is also evidence for genetic control of pathology due to S. mansoni, and linkage has been reported to a region containing the gene for the interferon-gamma receptor 1 subunit. There is some evidence for genetic control of filarial infection, though little information on filarial disease. Association studies have provided evidence for major histocompatibility complex control of pathology in schistosomiasis and onchocerciasis. Recent candidate gene studies suggest a role of other immune response genes in controlling helminth infection and pathology, but require replication. Identification of the genetic loci involved may be important in the understanding of helminth epidemiology and the mechanisms of resistance and pathology.
D000818:Animals; D000909:Antibodies, Helminth / Q000235:genetics / Q000276:immunology; D017164:Ascaris lumbricoides / Q000276:immunology; D001249:Asthma / Q000235:genetics / Q000276:immunology / Q000469:parasitology; D005368:Filariasis / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006680:HLA Antigens; D006373:Helminthiasis / Q000235:genetics* / Q000276:immunology; D006790:Host-Parasite Interactions / Q000235:genetics; D006801:Humans; D008285:Major Histocompatibility Complex; D012550:Schistosoma mansoni / Q000276:immunology
D000909:Antibodies, Helminth; D006680:HLA Antigens