TY - JOUR

T1 - Human Schistosoma haematobium antifecundity immunity is dependent on transmission intensity and associated with immunoglobulin G1 to worm-derived antigens

AU - Wilson, Shona

AU - Jones, Frances M.

AU - van Dam, Govert J.

AU - Corstjens, Paul L. A. M.

AU - Riveau, Gilles

AU - Fitzsimmons, Colin M.

AU - Sacko, Moussa

AU - Vennervald, Birgitte J

AU - Dunne, David W.

N1 - © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America.

PY - 2014

Y1 - 2014

N2 - BACKGROUND: Immunity that reduces worm fecundity and, in turn, reduces morbidity is proposed for Schistosoma haematobium, a parasite of major public health importance. Mathematical models of epidemiological trends suggest that antifecundity immunity is dependent on antibody responses to adult-worm-derived antigen.METHODS: For a Malian cohort (age, 5-29 years) residing in high-transmission fishing villages or a moderate-transmission village, worm fecundity was assessed using the ratio of urinary egg excretion to levels of circulating anodic antigen, a Schistosoma-specific antigen that is steadily secreted by adult worms. Fecundity was modeled against host age, infection transmission intensity, and antibody responses specific to soluble worm antigen (SWA), tegument allergen-like 1, and 28-kDa glutathione-S-transferase.RESULTS: Worm fecundity declined steadily until a host age of 11 years. Among children, host age and transmission were negatively associated with worm fecundity. A significant interaction term between host age and transmission indicates that antifecundity immunity develops earlier in high-transmission areas. SWA immunoglobulin G1 (IgG1) levels explained the effect of transmission on antifecundity immunity.CONCLUSION: Antifecundity immunity, which is likely to be protective against severe morbidity, develops rapidly during childhood. Antifecundity immunity is associated with SWA-IgG1, with higher infection transmission increasing this response at an earlier age, leading to earlier development of antifecundity immunity.

AB - BACKGROUND: Immunity that reduces worm fecundity and, in turn, reduces morbidity is proposed for Schistosoma haematobium, a parasite of major public health importance. Mathematical models of epidemiological trends suggest that antifecundity immunity is dependent on antibody responses to adult-worm-derived antigen.METHODS: For a Malian cohort (age, 5-29 years) residing in high-transmission fishing villages or a moderate-transmission village, worm fecundity was assessed using the ratio of urinary egg excretion to levels of circulating anodic antigen, a Schistosoma-specific antigen that is steadily secreted by adult worms. Fecundity was modeled against host age, infection transmission intensity, and antibody responses specific to soluble worm antigen (SWA), tegument allergen-like 1, and 28-kDa glutathione-S-transferase.RESULTS: Worm fecundity declined steadily until a host age of 11 years. Among children, host age and transmission were negatively associated with worm fecundity. A significant interaction term between host age and transmission indicates that antifecundity immunity develops earlier in high-transmission areas. SWA immunoglobulin G1 (IgG1) levels explained the effect of transmission on antifecundity immunity.CONCLUSION: Antifecundity immunity, which is likely to be protective against severe morbidity, develops rapidly during childhood. Antifecundity immunity is associated with SWA-IgG1, with higher infection transmission increasing this response at an earlier age, leading to earlier development of antifecundity immunity.

U2 - 10.1093/infdis/jiu374

DO - 10.1093/infdis/jiu374

M3 - Journal article

C2 - 25001462

VL - 210

SP - 2009

EP - 2016

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 12

ER -