Abstract
HIV-induced dysfunction of B-cells and antibody production may contribute to impaired control of HIV replication. One mechanism by which HIV may evade protective antibody responses is to reduce opsonophagocytic antibody responses against HIV antigens by impairing memory B-cell isotype switching to lgG2 antibody production. This would also have the effect of increasing susceptibility to infection by pneumococci and other encapsulated bacteria. This thesis addresses the impact of B-cell and follicular-helper (TFH) cell depletion and dysfunction on switching of pneumococcal polysaccharide antibodies to lgG2 in HIV-1Infection.
Original language | English |
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Qualification | Doctor of Philosophy |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 19 Aug 2016 |
Publication status | Unpublished - 2015 |