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Appetite suppressant for scavenger cells
Date:11/15/2012

This press release is available in German.

When infected with influenza, the body becomes an easy target for bacteria. The flu virus alters the host's immune system and compromises its capacity to effectively fight off bacterial infections. Now, a team of immunologists at the Helmholtz Centre for Infection Research (HZI) and cooperation partners has discovered that an immune system molecule called TLR7 is partly to blame. The molecule recognizes the viral genome and then signals scavenger cells of the immune system to ingest fewer bacteria. The researchers published their findings in the Journal of Innate Immunity.

The flu is not just a seasonal illness during the winter months. In the past, there have been several flu pandemics that have claimed the lives of millions. By now, we know that during the course of the disease, many people not only get sick from the flu itself but also from bacterial pathogens like the much-feared pneumococci, the bacteria causing pneumonia. In many cases, such "superinfections" can cause the disease to take a turn for the worse. In fact, during the Spanish Flu of 1918 to 1920, they were responsible for the majority of deaths. Why an infection with the flu virus increases the risk for superinfections is still poorly understood. Now, a group of scientists from HZI, the University Hospital of the Otto von Guericke University Magdeburg, the Essen University Hospital, the Karolinska Institute in Stockholm, Sweden, as well as further research institutions have discovered one more detail on how the virus manipulates the immune system.

They focused on TLR7, a molecule that is found in different cells of the body. TLR7 is capable of recognizing viral genetic material. As it turns out, TLR7 has an unwanted side effect, too: During a flu infection, it appears to undermine the body's innate ability to fight off ba
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Contact: Birgit Manno
Birgit.Manno@helmholtz-hzi.de
49-053-161-811-411
Helmholtz Centre for Infection Research
Source:Eurekalert  

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