Impairment of B cell trafficking and differentiation during HIV-1 infection

During the course of HIV-1 infection, several B cell dysfunctions occur as result of virus replication and indirect mechanisms of immunopathology. The B cells abnormalities include hypergammaglobulinemia, a decreased number of memory B cells, increased levels of activation markers on B cell surface and plasmacytosis. The molecular bases for these impairments are not fully characterized but may have relevance for designing functional HIV vaccines and improved treatment. In paper I the expression of chemokine receptors/chemokines important for B cell function was determined on cells from HIV-1 infected patients and controls. We studied the CXC chemokine receptor 4 (CXCR4), CXCR5, and CC chemokine receptor 7 (CCR7) and their respective ligands. We found a decreased expression of CXCR5 to be present on blood B cells from patients (P