title: Role of incidental and/or cured intestinal parasitic infections on profile of CD4+ and CD8+ T cell subsets and activation status in HIV-1 infected and uninfected adult Ethiopians.
abstract: Intestinal parasitic infections have been suggested to cause persistent immune activation leading to an unbalanced immune state. Such a state has been proposed to be a major factor in the pathogenesis of AIDS in an African context. The present study investigated the effect of incidental parasitic infection and treatment on the profile of T cell differentiation and activation markers on CD4+ and CD8+ T cells from HIV-1 infected and uninfected adult Ethiopians. Cryopreserved PBMCs from 64 subjects (41 HIV-negative and 23 HIV-positive) with follow-up visits at 6-monthly intervals were used to compare the effect of incidental intestinal parasites and their treatment upon T cell subset profiles and activation status. The samples were stained with antibodies to various T cell differentiation and activation markers allowing naive, memory, effector, memory/effector, activated and resting CD4+ and CD8+ T cell subsets to be quantified by triple-colour FACScan. Incidental intestinal parasitic infections resulted in a significant increase in memory CD4+ T cell numbers both in HIV-negative and HIV-positive subjects (P < 0.05). There was also a significant increase in the percentage of CD8+ HLA-DR+ T cells (P < 0.05) in HIV-positive subjects co-infected with parasites. In HIV-negative subjects, a significant decline in activated cells and a significant increase in resting CD8+ T cells (P < 0.05) was observed after treatment for parasites. These data suggest that intestinal parasitic infections could result in the alteration of T cell subset counts and also in the up-regulation of T cell activation markers in peripheral blood. Treatment of parasitic infections showed a tendency to reduce the activation suggesting that, together with other community based intervention strategies, such treatment could be used to down-regulate immune activation and hence protect the host from being easily attacked by HIV.
authors.affiliation: Gondar College of Medical Sciences, Department of Microbiology and Parasitology, Gondar, Ethiopia.
authors.forename: A
authors.initials: A
authors.lastname: Kassu
authors.forename: A
authors.initials: A
authors.lastname: Tsegaye
authors.forename: D
authors.initials: D
authors.lastname: Wolday
authors.forename: B
authors.initials: B
authors.lastname: Petros
authors.forename: M
authors.initials: M
authors.lastname: Aklilu
authors.forename: E J
authors.initials: EJ
authors.lastname: Sanders
authors.forename: A L
authors.initials: AL
authors.lastname: Fontanet
authors.forename: D
authors.initials: D
authors.lastname: Van Baarle
authors.forename: D
authors.initials: D
authors.lastname: Hamann
authors.forename: T F Rinke
authors.initials: TF
authors.lastname: De Wit
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D016022:Case-Control Studies; D005002:Ethiopia; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D015658:HIV Infections / Q000150:complications* / Q000276:immunology; D015497:HIV-1; D006801:Humans; D007411:Intestinal Diseases, Parasitic / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D018709:Statistics, Nonparametric; D016176:T-Lymphocyte Subsets / Q000276:immunology*