How to improve the harmful side-effects of flu
Due to the public health impact of influenza, there is a strong need to investigate and develop therapies that address our body’s response to viral infections, which may have an impact on the life of the virus.
The fellowship will specifically focus on Influenza A (H1N1), which was the most common cause of human influenza in 2009. The research will seek to explain the negative effects of oxidative stress induced by H1N1, which is caused by the interaction between highly reactive molecules, known as free radicals, and other molecules within the cells.
The stress is produced after part of the H1N1 flu virus is incorporated into infected cells. The research will investigate how this hampers the function and activity of the amiloride-sensitive epithelial sodium channel (ENaC) – one of the body’s ion channels, found in the tissue which lines the lungs.
When this is not functioning correctly, it can lead to the harmful side-effects caused by flu. The study will assess the impact in both a living organism (in vivo) and in an artificial environment (in vitro).
Up to date, we have been the first team to use the mouse adapted A/California/04/2009 Influenza H1N1 virus to conduct a preclinical trial of anti-viral treatment in order to understand how this strain is able to infect mice. We examined how two anti-viral drugs (oseltamivir and ribavirin) lessened Acute Lung Injury that occurs after Influenza infection. This project is in the final process of drafting for publication.
We have also conducted a proof of principle study in which we administered two antioxidants (Ascorbate and deferoxamine) in a combined fashion, to mice suffering from chlorine gas induced lung injury. The survival rate was increased 4-fold while all indexes of lung injury in the surviving mice were improved drastically. This work was published online in the beginning of December in the American Journal of Respiratory Cellular Molecular Biology.
Posted by Sotirios Zarogiannis