Flu's protective coat must melt to infect a cell

They found the viruses coat themselves in fatty material that hardens to a gel, protecting them in the cold.

This coating melts in the higher temperatures of the respiratory tract, allowing the virus to infect cells.

The US National Institutes of Health team hope their study, which features in the journal Nature Chemical Biology, could lead to new treatments.

The study results open new avenues of research for thwarting winter flu outbreaks

Dr Duane Alexander

National Institute of Child Health and Human Development

However, a UK expert said the discovery did not explain why some flu viruses also thrived in tropical climates.

The hard rubbery coating around the virus which forms in colder temperatures gives it the protection it needs to pass from person to person. The coating is so robust it can even resist to certain detergents.

However, once inside a host the virus can only infect a target cell once the coating has melted.

But this liquid phase is not tough enough to protect the virus against the elements, and so if the protective coating melts when the virus is outside the host, it dies.

Detailed fingerprint

Dr Duane Alexander, director of the National Institute of Child Health and Human Development, said: "The study results open new avenues of research for thwarting winter flu outbreaks.

"Now that we understand how the flu virus protects itself so that it can spread from person to person, we can work on ways to interfere with that protective mechanism."

The researchers used a sophisticated magnetic resonance technique to create a detailed fingerprint of how the flu virus's outer membranes responded to variations in temperature.

I don't think this study provides anything like a definitive answer on the spread of the virus

Professor John Oxford

Queen Mary College School of Medicine

The virus's outer membrane is composed chiefly of molecules known as lipids, such as oils, fats and cholesterol.

The researchers found that at temperatures slightly above freezing, this lipid covering solidified into a gel.

However, as temperatures approached 15.6C (60F) , the covering gradually thawed, eventually melting to a soupy mix.

The researchers concluded that temperatures in the spring and summer were too high to allow the viral membrane to enter its gel state.

As a result, at these temperatures the individual flu viruses would dry out and weaken - accounting for the end of the flu season.

Professor John Oxford, an expert in virology at Queen Mary College School of Medicine, London, said the paper was interesting, but it might be premature to draw firm conclusions.

He said: "If this is the case why do we get flu in tropical areas, where the temperature is 35C (95F) all the time?

"Places like Vietnam and Indonesia are predicted to be the epicentre of a new outbreak of pandemic flu."

Professor Oxford said researchers had tried to link flu infection definitively to cold weather since the great Russian outbreak of 1890, but had failed to come up with conclusive proof of a link.

"I don't think this study provides anything like a definitive answer on the spread of the virus - there must be some other factors that come into play," he said.