Mutated influenza virus sabotages lungs’ clearing mechanism
23 November 2010
A variant of last year’s pandemic influenza linked to fatal cases carried a mutation enabling it to infect a different subset of cells lining the airway, according to new research published in the Journal of Virology on 22 October by the Department of Medicine, the Medical Research Council National Institute for Medical Research and the University of Marburg.
The 2009 pandemic of H1N1 influenza caused thousands of deaths worldwide but the majority of cases were relatively mild. However, people infected with a variant of the virus, which carried a mutation termed D222G in a protein on its surface, were more likely to have a severe and fatal illness.
The new research shows that flu virus with the D222G mutation has an increased capacity to infect ciliated cells. These cells, found in the lining of the airway, have hair-like projections called cilia. The cilia sway back and forth to move mucus with trapped particles upward toward the mouth and this is normally swallowed or coughed up. When ciliated cells become infected, the cilia stop moving and this vital clearance function is impaired. Inhaled viruses and bacteria can then reach the lung more easily, where they can potentially cause pneumonia.
“This simple mutation, which swapped one building block of a virus protein for another, apparently resulted in a more virulent version of the H1N1 virus,” said lead author Professor Ten Feizi (Medicine). “If the mutant virus were to acquire the ability to spread more widely, the consequences could be very serious.”
— Sam Wong, Communications and Development
Tags: Faculty of Medicine, Medical Research Council
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