African Trypanosomosis Obliterates DTPa Vaccine-Induced Functional Memory So That Post-Treatment Challenge Fails to Trigger a Protective Recall Response.

Salivarian trypanosomes are extracellular parasites causing anthroponotic and zoonotic infections. Anti-parasite vaccination is considered the only sustainable method for global trypanosomosis control. Unfortunately, no single field applicable vaccine solution has been successful so far. The active destruction of the host's adaptive immune system by trypanosomes is believed to contribute to this problem. Here, we show that infection results in the lasting obliteration of immunological memory, including vaccine-induced memory against non-related pathogens. Using the well-established DTPa vaccine model in combination with a infection and a diminazene diaceturate anti-parasite treatment scheme, our results demonstrate that while the latter ensured full recovery from the infection, it failed to restore an efficacious anti- vaccine recall response. The DTPa vaccine failure coincided with a shift in the IgG1/IgG2a anti- antibody ratio in favor of IgG2a, and a striking impact on all of the spleen immune cell populations. Interestingly, an increased plasma IFNγ level in DTPa-vaccinated trypanosome-infected mice coincided with a temporary antibody-independent improvement in early-stage trypanosomosis control. In conclusion, our results are the first to show that trypanosome-inflicted immune damage is not restored by successful anti-parasite treatment.