| dc.description.abstract | Abstract
Epidemiological observations suggest that T cell immunity may be suppressed in malaria-endemic
areas. In vitro studies, animal models, and limited data in humans link immunosuppression with
malaria, malnutrition, and other parasitic infections. However, there are no data to determine
whether malaria-induced immunosuppression is significant in the long-term, or relative data
comparing it with other factors in malaria-endemic areas, so as to measure the impact of malaria,
other parasitic disease, nutritional status, age. and location on the acquisition and longevity of
IFN-γ responses in children in Kenya. We studied these factors in two cohorts of 1- to 6-year-old
children in a malaria-endemic area. T cell responses were induced by vaccination in one cohort,
and acquired as a result of natural exposure in a second cohort. Serial ELISPOT assays conducted
over a 1-year period measured the induction and kinetics of IFN-γ production in response to the
malaria Ag thrombospondin-related adhesion protein. Induced responses in both cohorts and the
longevity of response in the vaccinated cohort were fitted to potential explanatory variables.
Parasitemia was prospectively associated with reduced IFN-γ-producing T cells in both cohorts
(by 15-25%), and both parasitemia and episodes of febrile malaria were associated with 19 and
31% greater attrition of T cell responses, respectively. Malaria may reduce the efficacy
vaccinations such as bacillus Calmette-Guérin and investigational T cell-inducing vaccines, and
may delay the acquisition of immunity following natural exposure to malaria and other pathogens. | en_US |
