This release is available in German.
Viruses are microscopically sized parasites. They plant their genes in the cells of their victim in order to 'reprogram' them. The infected cells then no longer produce what they need to live, making lots of new viruses instead.
Luckily, in most cases this hostile takeover does not go unnoticed. This is ensured by the cells' own sensors that recognise alien genetic material. One of them is RIG-I. When RIG-I encounters virus genes, it ensures that the body releases interferon. The interferon then in turn puts killer cells on combat standby, which then destroy the infected cells.
Yet this is only part of the truth. 'According to our results RIG-I appears to play a far more prominent role in the defence against viruses than was previously thought,' Dr. Jrgen Ruland from the University Hospital Rechts der Isar at the Technical University of Munich explains. As a result, many virus infections are accompanied by a high temperature. That is also what happens with influenza, for example. This symptom cannot be explained by interferon release alone.
In most cases it is cytokines which trigger the fever. 'We have now been able to show, for the first time, that RIG-I also cranks up the production of a central cytokine in the case of a virus infection,' Dr. Hendrik Poeck explains. He and his colleagues Dr. Michael Bscheider and Dr. Olaf Gro are the primary authors of the study. This is a reference to interleukin 1, probably the most important cytokine known today.
Do cytokines cause more severe courses of a disease?
When RIG-I comes into contact with a virus gene, it does two things. On the one hand, it ensures that certain immune cells produce pro-interleukin, the precursor of interleukin 1, en masse. At the same time it activates an enzyme via a complicated signalling pathway whi
|Contact: Veit Hornung|
University of Bonn