Scientists have discovered that a biological molecule important in cell growth (STAT3) is also critical in protecting us against infection – so much so that we would be unable to fight the common flu virus without it. Their discovery could pave the way to the development of new therapeutics charged with restoring our natural immunity to a whole spectrum of viruses that have evolved ‘roadblocks’ to the immune response.
The team behind the work was led by Assistant Professor in Immunology at Trinity College Dublin, Dr Nigel Stevenson, who is based in the Trinity Biomedical Sciences Institute. The findings have recently been published in the journal Cellular and Molecular Life Sciences CMLS.
In a world of newly emerging viral infections such as SARS, ZIKA and Ebola, the importance of understanding how viruses target our immune system, and the need to develop new therapies to cure and protect us, has never been greater.
During any viral infection our cells produce an immune molecule called Interferon, which essentially ‘interferes’ with the battle plans of attacking viruses — preventing them from replicating in our bodies. When our cells are stimulated by Interferon a cascade of molecules within our cells is activated like a series of dominos. When the final one falls, the cell should be able to clear the viral infection. This cascade of molecules is termed a signalling pathway as it passes the ‘danger signal’ of viral infection through the cell.
Cartoonist Lisa Brown’s depiction of the constant battle waging in our bodies between our immune system and viral infections.
The Interferon signalling pathway initiates the production of several hundred immune molecules that act to destroy viruses and amplify our immune response against them. However, as we know, many viruses are not cleared by our natural immune response and can often cause serious illness. Immunologists from Trinity, wondering how viruses suppress the immune response, have discovered that they have evolved numerous methods to inhibit these signalling pathways and thus block responses to Interferon.
Indeed, over the past few years, Dr Stevenson and his team had discovered that Hepatitis C Virus (HCV) and Respiratory Syncytial Virus (RSV), among others, specifically target the Interferon signalling pathway which helps them avoid being naturally cured by our immune systems.
Scientists had, until now, believed they fully understood how the Interferon signalling pathway worked, but by using a series of viral infections and cutting-edge molecular techniques, Dr Stevenson’s team discovered a new anti-viral role for STAT3.
Thomas Deane, Press Officer for the Faculty of Engineering, Mathematics and Science | [email protected] | 01 896 4685
Trinity College Dublin