# Viral interactions with host factors (TIM-1, TAM -receptors, Glut-1) are related to the disruption of glucose and ascorbate transport and homeostasis, causing the haemorrhagic manifestations of viral haemorrhagic fevers

## TL;DR

This paper explores how viruses disrupt glucose and ascorbate transport, leading to hemorrhagic symptoms in viral fevers.

## Contribution

It identifies specific host factors like TIM-1, TAM receptors, and Glut-1 involved in viral pathogenesis.

## Key findings

- Viral interactions with TIM-1 and TAM receptors disrupt Glut-1 expression.
- Glut-1 is linked to glucose and ascorbate transport in susceptible species.
- Disruption of these transporters may cause hemorrhagic symptoms in viral infections.

## Abstract

The haemorrhagic features of viral haemorrhagic fevers may be caused by common patterns of metabolic disturbances of the glucose and ascorbate homeostasis. Haemorrhages and vasculature disfunctions are a clinical feature not only of viral haemorrhagic fevers, but also in scurvy, diabetes and thrombotic microangiopathic haemolytic anaemia. Interestingly, the expression of glucose and ascorbate transporter Glut-1 on the erythrocyte membrane is associated with the inability to synthesize ascorbate and is restricted to that very species that are susceptible to Filoviruses (primates, humans and fruit bats). Glut-1 may play a pivotal role in haemorrhagic fever pathogenesis. TIM-1 and TAM receptors have been recognized to enhance entry of Ebola, Lassa and Dengue viruses and viral interferences with TIM-1 could disturb its function, disturbing the expression of Glut-1.