The structure of the TfR1 receptor

Stephen Harrison, Children's Hospital Boston and Howard Hughes Medical Institute

Researchers have identified a receptor through which haemorrhagic fever viruses enter and attack the body’s cells. The discovery may form the basis of new treatment strategies for these deadly diseases.

The study published online in Nature yesterday (7 February) also shows how iron deficiency can affect the severity of haemorrhagic fevers, suggesting that iron supplements may make people less susceptible to the viruses.

Haemorrhagic fevers are a group of illnesses caused by several distinct families of viruses, which damage multiple organs and can cause bleeding under the skin, in the mouth, eyes or ears.

Acute haemorrhagic fevers — such as the Argentinian, Bolivian, Brazillian and Venezuelan fevers — have a mortality rate of 30 per cent.

The researchers investigated 'new world' haemorrhagic fevers, specifically the Machupo virus, which causes Bolivian hemorrhagic fever.

They found that these viruses enter human cells via a well-known receptor, called TfR1, which enables the cells to take up iron. The authors say blocking this receptor could prevent infection.

TfR1 is particularly abundant on the surface of immune cells — those mobilised to fight infections — making them especially vulnerable. This may explain why the diseases are so deadly.

The team, led by Hyeryun Choe of the Harvard Medical School, United States, found that adding iron to cell cultures made them less susceptible to infection.

If an infected person has low iron-levels they may have more severe disease symptoms, says Choe.    

She told SciDev.Net that outbreaks of new world haemorrhagic fever mostly occur in poor rural areas, where people are often deficient in micronutrients, including iron.

But she stressed that the research was specific to new world viruses, rather than old world viruses that affect Africa, such as the Lassa fever virus or those causing Ebola or Rift Valley Fever.

Reference: Nature doi: 10.1038/nature05539 (2007)

Link to full paper in Nature