Herpes zoster in the context of varicella vaccination - An equation with several variables.

Background: Varicella and herpes zoster (HZ), diseases both caused by the varicella zoster virus (VZV), are vaccine-preventable. However, the hypothesis that childhood varicella vaccination may increase the incidence of HZ hinders varicella universal routine vaccination (URV) implementation in many countries.

Methods: This non-systematic and narrative review of the literature considers the burden of varicella and HZ, and the effectiveness of the respective vaccines.

Maintenance of B cells during chronic murine Trypanosoma brucei gambiense infection.

African trypanosomosis is a debilitating parasitic disease occurring in large parts of sub-Saharan Africa. Trypanosoma brucei gambiense accounts for 98% of the reported HAT infections and causes a chronic, gradually progressing disease. Multiple experimental murine models for trypanosomosis have demonstrated inflammation-dependent apoptosis of splenic follicular B (FoB) cells and the destruction of B-cell memory against previously encountered pathogens.

IFN-γ mediates early B-cell loss in experimental African trypanosomosis.

African trypanosomes infect humans and animals throughout the African continent. These parasites maintain chronic infections by various immune evasion strategies. While antigenic variation of their surface coat is the most studied strategy linked to evading the host humoral response, African trypanosomes also induce impaired B-cell lymphopoiesis, the destruction of the splenic B-cell compartment and abrogation of protective memory responses.

Curative drug treatment of trypanosomosis leads to the restoration of B-cell lymphopoiesis and splenic B-cell compartments.

African trypanosomosis is a parasitic disease affecting both humans (sleeping sickness) and animals (nagana). In murine trypanosomosis, the B-cell compartment is rapidly destroyed after infection. In addition, B-cell lymphopoiesis in the bone marrow is abrogated, B-cell subsets in the spleen are irreversibly depleted, and B-cell memory is destroyed.