Epstein-Barr virus (EBV) establishes a chronic infection, usually effectively controlled by the cellular immune response. However, EBV has the potential to escape immune control, such as during malaria exposure, or modulate the immune response. In this study, immune control of EBV was examined in Gambian children in two situations: during malaria exposure and early after EBV infection. Additionally, EBV infection may also inhibit vaccine induced antibody responses, hence its impact on a childhood pentavalent vaccine was studied, but infection had no effect. In contrast to historical studies, acute malaria infection was not associated with impaired immunity to EBV, a finding potentially explained by the declining malaria exposure in The Gambia. Children recently infected with EBV had evidence of activated EBV-specific T-cell responses, with latent and lytic epitope-specific responses of equal magnitude. Several donors identified as undergoing primary asymptomatic EBV infection had virus genome loads equivalent to those of acute infectious mononucleosis (AIM) patients. In contrast to AIM patients they did not show a peripheral lymphocytosis but did have significant expansions of activated EBV-specific CD8+ T-cells, which were lower or perhaps more focused than in AIM patients, suggesting that the highly expanded T-cell populations and not virus load drives AIM pathogenesis.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:571837 |
| Date | January 2013 |
| Creators | Jayasooriya, Shamanth |
| Publisher | University of Birmingham |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://etheses.bham.ac.uk//id/eprint/4173/ |
Page generated in 0.0014 seconds