This news could help in solving a few unanswered queries regarding H1N1. A team of study authors from the Hospital Clinico Universitario de Valladolid in Spain, Toronto’s University Health Network and the University of Toronto claim to have discovered the first possible immunological trace of why a few people develop acute pneumonia when they are supposedly infected by the pandemic H1N1 virus.
The study included around 20 hospitalized patients, 15 outpatients and 15 control patients in around 10 Spanish Hospitals during the initial pandemic upsurge in July and August 2009. The study authors examined their diverse levels of regulating molecules. The experts claimed to have discovered elevated levels of a molecule known as interleukin 17 in the blood of acute H1N1 patients and low levels in patients suffering from the mild form of the disease.
Interleukin 17 is supposedly generated by the body. This molecule also appears to be significant in the standard regulation of white blood cells which could combat infection and disease. In a few situations, the molecule becomes unmanageable, thereby apparently resulting in inflammation and autoimmune diseases. The study is said to refer to Th1 and Th17 hypercytokinemia as a premature host response signature in acute pandemic influenza.
Dr. David Kelvin, the leader of the Canadian team, a professor of immunology at the University of Toronto and head of the experimental therapeutics division, Toronto General Hospital Research Institute, University Health Network, commented, “In rare cases, the virus causes lung infections requiring patients to be treated in hospital. By targeting or blocking TH17 in the future, we could potentially reduce the amount of inflammation in the lungs and speed up recovery.”
Kelvin observed that nevertheless, an investigation to verify who appears to have elevated levels of the molecule could be feasible in the near future.
He added, “A diagnostic test could let us know early who is at risk for the severe form of this illness quickly.”
He mentioned that high levels could point out towards the malfunction of the immune system to get rid of the virus, comparable to what occurred in the 1918 Spanish flu when a large number of deaths took place owing to a lethal influenza A virus strain of subtype H1N1.
The study is published in the Journal of Critical Care.