The results of recent research into the avian influenza H5N1 virus might explain why it has difficulty spreading from human to human and it appears to have developed a genetically distinct variant.
An analysis of more than 300 H5N1 samples collected from infected birds and people between 2003 and 2005 indicates that a genetically different variant arose in 2005. All cases of human infection prior to 2005 were the result of a subtype of H5N1 which infected people in Vietnam, Cambodia and Thailand. Last year, a new variant emerged in people in Indonesia. Researchers indicate that either subtype could mutate into a form which could cause a human pandemic. They stress, however, that currently the viruses remain incapable of spreading easily between humans.
Results reported in the March 22, 2006 issue of the journal Nature might explain why. Japanese researchers led by Kyoko Shinya at the University of Wisconsin and the University of Tokyo have discovered that the receptors necessary for the attachment of the avian influenza viruses, designated alpha 2,3, are found deep in the lungs of humans rather than along the upper respiratory tract where the alpha 2,6 receptors for human flu viruses are found. For the virus to spread easily between humans it would have to mutate to a form able to attach to the receptors in the upper respiratory tract.
Additional research conducted in the Netherlands at Erasmus Medical Center by Thijs Kuiken and colleagues and published online in Science found that the avian H5N1 has an affinity for alveolar macrophages. This may account for the inflammatory response observed in fatal human cases of H5N1 infections that resulted in excessive pulmonary fluid.
Sources:
BBC, March 21, 2006
The Washington Post, March 23, 2006