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(Ivanhoe Newswire) -- A team of Canadian and Spanish scientists has found a potential immunological clue to why some people develop severe, sometimes fatal, pneumonia when infected by the H1N1 virus.
The study analyzed different levels of regulating molecules for 20 hospitalized patients, 15 outpatients and 15 control subjects in 10 Spanish hospitals during the first H1N1 wave in July and August 2009. Researchers from the Hospital Clinico Universitario de Valladolid in Spain and the University Health Network in Canada found high levels of the interleukin 17 molecule in the blood of patients with severe H1N1, and low levels in patients with the mild form of the disease.
Interleukin 17 is produced by the body and is important in the regulation of white blood cells, which fight infection and disease. In certain circumstances, however, the molecule goes "out of control," leading to inflammation and autoimmune disease.
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"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," Dr. David Kelvin, Head of the Experimental Therapeutics Division, Toronto General Hospital Research Institute, University Health Network and Professor of Immunology, University of Toronto, was quoted as saying.
Dr. Kelvin noted that a test to determine who has high levels of the molecule is possible in the near future. "A diagnostic test could let us know early who is at risk for the severe form of this illness quickly," he said, adding that high levels would indicate a failure of the immune system to eliminate the virus, similar to what happened during the 1918 Spanish flu when huge numbers of deaths occurred due to a deadly influenza A virus strain of subtype H1N1.
Dr. Jesus Bermejo-Martin, coordinator of the Spanish team, thinks that identifying drugs able to regulate the activity of IL-17 may provide alternative treatments for patients with severe H1N1.
SOURCE: Journal of Critical Care, December 2009
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