Erythrophagocytosis of desialylated red blood cells is responsible for anaemia during Trypanosoma vivax infection

Summary Trypanosomal infection‐induced anaemia is a devastating scourge for cattle in widespread regions. Although Trypanosoma vivax is considered as one of the most important parasites regarding economic impact in Africa and South America, very few in‐depth studies have been conducted due to the difficulty of manipulating this parasite. Several hypotheses were proposed to explain trypanosome induced‐anaemia but mechanisms have not yet been elucidated. Here, we characterized a multigenic family of trans‐sialidases in T. vivax, some of which are released into the host serum during infection. These enzymes are able to trigger erythrophagocytosis by desialylating the major surface erythrocytes sialoglycoproteins, the glycophorins. Using an ex vivo assay to quantify erythrophagocytosis throughout infection, we showed that erythrocyte desialylation alone results in significant levels of anaemia during the acute phase of the disease. Characterization of virulence factors such as the trans‐sialidases is vital to develop a control strategy against the disease or parasite. Animal trypanosomiasis remains by far the most detrimental animal parasitic disease on the African and South American continents. In this current study, we aimed to elucidate the underlying mechanism of anaemia, the major and poorly understood physiopathological trait of the disease. For the first time, we demonstrated that sialidase enzymes released by the parasite in the bloodstream desialylate glycoproteins on the erythrocyte surface. This erythrocyte surface desialylation is a major event triggering erythrophagocytosis and subsequent anaemia in Trypanosoma vivax infection.