The H5N1 influenza strain struggles to infect cells high up in the human airway, significantly limiting the extent to which victims can pick up the virus and pass it on by coughing and sneezing, according to research. The findings, from separate teams in the United States and the Netherlands, suggest that H5N1 will probably have to evolve substantially if it is to become easily transmissible between people; the key step that would make a pandemic possible.

The research also highlights several critical mutations that would ring alarm bells if spotted in virus samples, allowing for improved surveillance of the threat it poses to humans.

While the H5N1 virus is highly virulent when contracted by humans, with 184 cases and 103 deaths confirmed by the World Health Organisation, it does not easily infect people and all the victims so far picked it up by direct contact with birds.

This resilience to H5N1 stems from the way the virus binds to cells in the airway, the new studies indicate. While ordinary human strains of influenza readily infect cells in the windpipe, only cells much deeper inside the lungs have the right receptors that allow H5N1 to dock with them. This is important for two reasons: the upper airway is more likely to be exposed to the virus than the inner pockets of the lungs, and infections in the windpipe are also more readily passed on.

When the virus is present only in the lower respiratory tract, it is unlikely to be released by coughing and sneezing. People with upper airway infections, however, are likely to expel millions of virus particles with every splutter.

“Deep in the respiratory system, cell receptors for avian viruses, including avian H5N1 viruses, are present,” said Yoshihiro Kawaoka, of the University of Wisconsin-Madison, whose study is published today in the journal Nature.

“But these receptors are rare in the upper portion of the respiratory system. For the viruses to be transmitted efficiently, they have to multiply in the upper portion of the respiratory system so that they can be transmitted by coughing and sneezing.

“Our findings provide a rational explanation for why H5N1 viruses rarely infect and spread from human to human, although they can replicate efficiently in the lungs.”

The second study, led by Thijs Kuiken, of the Erasmus Medical Centre in Rotterdam, reached similar conclusions and is published in the journal Science. It found that the airways of cats and ferrets are affected by H5N1 in similar fashion to humans, making both good animal models for further research.

Dr Kawaoka said that the research pinpoints several key mutations, in the haemagglutinin protein that the virus uses to bind to cells, which would be of grave concern if they were to be identified in H5N1. “Identification of H5N1 viruses with the ability to recognise human receptors (in the upper airway) would bring us one step closer to a pandemic strain,” he said. “Recognition of human receptors can serve as molecular markers for the pandemic potential of the isolates.

“Mutations in the haemagglutinin for avian H5N1 viruses to recognise human receptors are needed for the virus to become a pandemic strain. No one knows whether the virus will evolve into a pandemic strain, but flu viruses constantly change. Certainly, multiple mutations need to be accumulated for the H5N1 virus to become a pandemic strain.” The results come days after a team in the US identified that the virus has split into two distinct genetic subtypes, widening the gene pool from which a pandemic strain might emerge.

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