Age‐dependency of infection status and serum antibody levels in human whipworm (Trichuris trichiura) infection

Abstract

This study examines the age-dependency of the relationships between human infection with whipworm (Trichuris trichiura) and parasite-specific antibody level measured by ELISA against an extract of adult worms after preincubation of the sera with Ascaris lumbricoides adult worm extract. The convex age-profile of parasite infection intensity is shown to be mirrored by an age-dependent change in age-class mean levels of IgG (all subclasses except IgG3), IgA, IgM and IgE. Mean antibody levels rise with increasing acquisition of infection in childhood and decline as the intensity of infection falls in adulthood. Immunoblot analysis of selected sera from different age-classes indicates that antigen recognition is similarly dependent on infection intensity. In individual children, antibody levels correlate positively with acquisition of infection, consistent with a simple model of antigen dosage specifying the magnitude of the humoral immune response. In adults, IgG4 correlates positively and IgA negatively with intensity of infection, suggesting involvement of these isotypes in functional roles of immune blockade or effector mechanisms, respectively.

Trichuris Burdens in Zoo-Housed Colobus guereza

“…Researchers in previous studies documented that burdens of Trichuris spp. are significantly higher in children than in adults, which they suggest is a consequence of age-dependent immunity response rather than decreased exposure with age (Macaca mulatta, Knezevich 1998; Homo sapiens, Bundy et al 1991).…”

Immunoepidemiology ofWuchereria bancroftiInfection: Parasite Transmission Intensity, Filaria-Specific Antibodies, and Host Immunity in Two East African Communities

“…Recent theoretical work has suggested that protective immunity in lymphatic filariasis may be dependent on the community transmission intensity, such that acquired immunity is manifest only in areas where there is higher transmission (24). Taken together, these observations suggest that (i) age-depen-dent associations between immune response levels and infection intensities can be expected to vary for communities with different mean transmission intensities and (ii) that taking a comparative immunoepidemiological approach to assessing age copatterns for communities in which transmission intensity differs is necessary for identifying and evaluating the role of protective immunity in regulating filarial infection in humans (3,14,16,17,24,25,27,28,48).…”

“…More specifically, it is hypothesized that the correlation between immune responses and infection intensity changes with both transmission intensity and host age; the association is expected to be positive in young children because both infection and immune responses reflect exposure, but as the hosts age, the association becomes negative as the immune response gained via cumulative exposure starts to regulate worm intensities (3,28,51). Implicit in this hypothesis is that this epidemiological age effect of acquired protective immunity should be manifest or should be greater in communities with higher transmission intensities (1,48).…”

“…The immunoepidemiological rationale for comparing age intensities of infection with corresponding age profiles of specific antibody responses in communities with different transmission intensities is that any intercommunity discordance between such profiles, especially in older subjects, is thought to provide not only a more direct sign of the occurrence of acquired immunity (3,10,27,28,46,48) but also identification of which of the specific immune components examined may potentially be a marker of such immunity. More specifically, it is hypothesized that the correlation between immune responses and infection intensity changes with both transmission intensity and host age; the association is expected to be positive in young children because both infection and immune responses reflect exposure, but as the hosts age, the association becomes negative as the immune response gained via cumulative exposure starts to regulate worm intensities (3,28,51).…”

“…These studies unambiguously showed that W. bancrofti infection can induce strong antibody responses (4,29,32,42,47), but protective responses have not been conclusively identified yet. Recent theoretical analysis and evidence from other helminth infections (3,9,27,28,35,36) suggest that one reason for this situation in the study of filariasis could be the paucity of studies that have used an immunoepidemiological perspective to investigate the role of acquired immunity in influencing parasitic infection patterns in host communities in areas where the organism is endemic. In particular, this perspective, which attempts to link observed individual host immune responses to epidemiological patterns, has shown how observation of an increasingly negative correlation between the levels of an immune response and the intensities of infection with increasing host age could indicate a protective role for the response being examined (10,27,(48)(49)(50).…”