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

Shona Wilson, Frances M. Jones, Govert J. van Dam, Paul L. A. M. Corstjens, Gilles Riveau, Colin M. Fitzsimmons, Moussa Sacko, Birgitte J Vennervald, David W. Dunne

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

29 Citationer (Scopus)

Abstract

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.

OriginalsprogEngelsk
TidsskriftThe Journal of Infectious Diseases
Vol/bind210
Udgave nummer12
Sider (fra-til)2009-2016
Antal sider8
ISSN0022-1899
DOI
StatusUdgivet - 2014

Citationsformater