Given that at least 30% of second stage sleeping sickness patients displayed elevated levels of anti-MBP autoantibodies in circulation posttreatment, likely as a result of treatment failure, we next decided to explore whether suramin treatment, used in experimental infections to clear T. brucei infections [18,80], prevented the accumulation of GL7+ CD95+ GC-like phenotype and IgG deposition in the brain. The gene discussed is MBP; the disease is human African trypanosomiasis.