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Infect. Immun. doi:10.1128/IAI.00970-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Immunoepidemiology of Wuchereria bancrofti infection: parasite transmission intensity, filarial-specific antibodies, and host immunity in two East African communities

Department of Medical Microbiology, University of Nairobi, PO Box 19676, Nairobi, Kenya; Department of Infectious Diseases Epidemiology, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom; Department of Epidemiology, Institute of Public Health, University of Copenhagen, Blegdamsvej 2, 2200 Copenhagen, Denmark; National Institute for Medical Research, PO Box 9653, Dar es Salaam, Tanzania; DBL – Institute for Health Research and Development, Jaegersborg Alle 1D, 2920 Charlottenlund, Denmark

^* To whom correspondence should be addressed. Email: e.michael{at}imperial.ac.uk.

	Abstract

We compared age profiles of infection and specific antibody intensities in two communities with differing transmission levels from East Africa to examine the contribution of humoral responses in human immunity to the vector-borne helminth, Wuchereria bancrofti. Worm intensities were higher and exhibited a non-linear age pattern in the high transmission community of Masaika, in contrast to the low but linearly increasing age-infection profile observed for the low transmission community of Kingwede. Mean levels of specific IgG1, IgG2, IgG4 and IgE were also higher in Masaika but the IgG3 response was intriguingly higher in Kingwede. Age-antibody patterns differed between the two communities but in a manner apparently contrary to a role in acquired immunity when assessed using simple correlation methods. By contrast, multivariate analyses showed that the antibody response to infection may be classified into three types, and that two of these, a IgG3-type response and a response measuring a trade-off in host production of IgG4 and IgG3 versus IgG1, IgG2 and IgE, had a negative effect on Wuchereria circulating antigen levels in a manner supporting a role for these responses in the generation of acquired immunity to infection. Mathematical modelling supported the conclusions from empirical data analyses that variations in both transmission and worm intensity can explain community differences in the age profiles/impacts of these antibody types. This study has shown that parasite specific antibody responses may be associated with the generation of acquired immunity to human filarial infection, but in a form, which is dependent on worm transmission intensity and interactions between immune components.