A comparison of epstein‐barr virus‐specific T‐cell immunity in malaria‐endemic and ‐nonendemic regions of Papua New Guinea

Abstract

Epstein-Barr virus genome-positive Burkitt's lymphoma is endemic in Africa and Papua New Guinea and in both countries the tumour is restricted to regions with holoendemic malaria. The present work has compared groups of healthy indigenous individuals living in malarious and non-malarious regions of Papua New Guinea for Epstein-Barr virus-specific T-cell-mediated immunity using the in vitro regression assay. Residents of the malarious region (55 tested), when compared with either residents of the non-malarious area (35 tested) or Caucasian controls (27 tested) showed a significant (p less than 0.0001) impairment of virus-specific T-cell immunity but no obvious disturbance (p greater than 0.05) of anti-viral antibody titres. These results may be important in explaining the postulated role of malarial infection as a co-factor in the pathogenesis of Burkitt's lymphoma.

Holoendemic Malaria Exposure Is Associated with Altered Epstein-Barr Virus-Specific CD8 + T-Cell Differentiation

“…Such immunologic perturbations within the EBV-specific CD8 ϩ T-cell compartment could predispose to the functional deficits that accompany eBL (46). Second, our study addresses the long-standing question of whether eBL is associated with a generalized, malaria-induced suppression of T-cell immunity (21,22,47). Our data demonstrate that EBV-specific, but not CMV-specific or total, CD8 ϩ T-cell populations show significant differences associated with malaria exposure.…”

“…Indeed, these properties underlie the hypothesis that P. falciparum malaria suppresses immunity to EBV during coinfection. In the early 1980s, a series of seminal studies demonstrated that lymphocytes from malaria-infected individuals were unable to control the proliferation of EBV-transformed B cells in relatively crude regression assays (21,22). Although these observations suggest that P. falciparum malaria infection disrupts EBV-specific immunity, the effector cells or mediators responsible for controlling EBV-infected B-cell growth were not identified, and overall immune competence was not assessed in the small number of individuals studied.…”

Phase I Trial of a CD8+T-Cell Peptide Epitope-Based Vaccine for Infectious Mononucleosis

“…The initial HLA screening was performed by fluorescence-activated cell sorter (FACS) analysis using the HLA B*0801 monoclonal antibody (clone 59HA-1; One Lambda Inc.) and was later confirmed by full class I tissue typing (Princess Alexandra Hospital tissue typing facility, Brisbane, Australia). Serological testing for EBV capsid antibody (VCA) was initially done by immunofluorescence microscopy (37) and later confirmed by enzyme-linked immunosorbent assay specific for VCA immunoglobulin G (IgG) and IgM and EBNA IgG (Queensland Medical Laboratory, Brisbane, Queensland, Australia). The inclusion criteria for the trial were EBV-seronegative and HLA B*0801-positive status.…”

Epstein-Barr Nuclear Antigen 1-Specific CD4+ Th1 Cells Kill Burkitt’s Lymphoma Cells

“…Holoendemic malarial infection is thought to facilitate this oncogenic process. Therefore, BL occurs with increased incidence rate in children in Sub-Saharan Africa (3), in South America (4), and in Papua New Guinea (5). In addition, BL is increased in AIDS patients (6 -8).…”