Thus, filoviruses in those species expressing the glucose and ascorbate transporter Glut-1 on erythrocytes and unable to synthesize ascorbate, would cause pathophysiological changes that account for the severity of the filoviral haemorrhagic fevers, by means of a virus-driven disruption or overwhelming of ascorbate and/or glucose homeostasis. Here, SLC2A1 is linked to hemorrhagic fever.