Membrane damage produced by parvovirus B19 tags erythrocytes as senescent and is an aggravating cause of virus-triggered anemias

Abstract

Parvovirus B19 (B19V) is the causative agent of erythema infectiosum and other diseases, including aplastic anemia in individuals with underlying hemolytic disorders such as sickle cell disease, spherocytosis or thalassemia. It has been well-established that B19V affects the development of red blood cells (RBC) by infecting erythroid progenitor cells (EPC) in the bone marrow. The first step in B19V infection is the binding of the virion to the glycosphingolipid (GSL) globoside (Gb4) on the EPC surface and temporarily stopping erythropoiesis. Although this infection is tolerated well by healthy patients, it can lead to severe aplastic crises in anemia patients. Gb4 is also the most abundant neutral glycolipid in the erythrocyte membrane. It has been documented that B19V and its virus-like particles (VLP) produce hemagglutination of RBCs. We hypothesized that B19V binding to the RBC membrane must induce changes impairing its function and reducing the cell’s half-life, being an aggravating cause of anemias produced by B19V. Here, we present optic and electronic microscopy evidence of morphological changes on the surface of the RBC produced by the presence of B19V VLP, supporting this hypothesis.